Search Criteria: Research Area is "Neurobiology Research: Behavioral and Learning Defects"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002052 | B6.129P2-Apoetm1Unc/J | Level 1 |
| Mice homozygous for the Apoetm1Unc mutation show a marked increase in total plasma cholesterol levels that are unaffected by age or sex. Fatty streaks in the proximal aorta are found at 3 months of age. The lesions increase with age and progress to lesions with less lipid but more elongated cells, typical of a more advanced stage of pre-atherosclerotic lesion. Moderately increased triglyceride levels have been reported in mice with this mutation on a mixed C57BL/6 x 129 genetic background. Aged APOE deficient mice (>17 months) have been shown to develop xanthomatous lesions in the brain consisting mostly of crystalline cholesterol clefts, lipid globules, and foam cells. Smaller xanthomas were seen in the choroid plexus and ventral fornix. Recent studies indicate that APOE deficient mice have altered responses to stress, impaired spatial learning and memory, altered long term potentiation, and synaptic damage. | ||
| 000651 | BALB/cJ | Level 1 |
| BALB/c mice are particularly well known for the production of plasmacytomas following injection with mineral oil forming the basis for the production of monoclonal antibodies. Although not all BALB/c substrains have been examined for plasmacytoma induction, substrains derived from the Andervont (An) lineage (which includes BALB/cByJ) typically are susceptible, while those descended from BALB/cJ are resistant (see: Potter M ,1985). Mammary tumor incidence is normally low but infection with mammary tumor virus by fostering to MMTV+ C3H mice dramatically increases tumor number and age of onset. BALB/c mice develop other cancers later in life including reticular neoplasms, primary lung tumors, and renal tumors. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in both BALB/cJ and BALB/cByJ substrains.
White et al. reported a variation in thioglycolate medium-induced peritoneal leukocyte recruitment in 4 analyzed s
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| 000664 | C57BL/6J | Level 1 |
| C57BL/6 is the most widely used inbred strain. It is commonly used as a general purpose strain and background strain for the generation of congenics carrying both spontaneous and induced mutations. Although this strain is refractory to many tumors, it is a permissive background for maximal expression of most mutations. C57BL/6J mice are used in a wide variety of research areas including cardiovascular biology, developmental biology, diabetes and obesity, genetics, immunology, neurobiology, and sensorineural research. C57BL/6J mice are also commonly used in the production of transgenic mice. Overall, C57BL/6 mice breed well, are long-lived, and have a low susceptibility to tumors. Primitive hematopoietic stem cells from C57BL/6J mice show greatly delayed senescence relative to BALB/c and DBA/2J. This is a dominant trait. Other characteristics include: 1) a high susceptibility to diet-induced obesity, type 2 diabetes, and atherosclerosis; 2) a high incidence of microphthalmia and other a
..... For more information please see the full descriiption on the strain data sheet | ||
| 002810 | B6CBA-Tg(HDexon1)62Gpb/1J | Level 3 |
| This line is transgenic for the 5' end of the human HD gene carrying (CAG)115-(CAG)150 repeat expansions. The transgene is ubiquitously expressed. Transgenic mice exhibit a progressive neurological phenotype that mimics many of the features of HD, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures, as well as nonmovement disorder components, including unusual vocalization. They urinate frequently and exhibit loss of body weight and muscle bulk through the course of the disease. Neurologically they develop Neuronal Intranuclear Inclusions (NII) which contain both the huntingtin and ubiquitin proteins. Previously unknown, these NII have subsequently been identified in human HD patients. The age of onset of HD symptoms is reported to occur between nine and 11 weeks. Commonly known as the "R6/2" strain.
Transgenic mice develop hyperglycemia by 12 weeks of age with a corresponding decrease in insulin levels. Pancreatic beta cells devel
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| 006494 | B6CBA-Tg(HDexon1)62Gpb/3J | Level 3 |
| This line is transgenic for the 5' end of the human HD gene carrying less than (CAG)150 repeat expansions. The transgene is ubiquitously expressed. Transgenic mice exhibit a progressive neurological phenotype that mimics many of the features of HD, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures, as well as nonmovement disorder components, including unusual vocalization. They urinate frequently and exhibit loss of body weight and muscle bulk through the course of the disease. Neurologically they develop Neuronal Intranuclear Inclusions (NII) which contain both the huntingtin and ubiquitin proteins. Previously unknown, these NII have subsequently been identified in human HD patients. The age of onset of HD symptoms is reported to occur between 9 and 11 weeks. Commonly known as the "R6/2" strain. Transgenic mice develop hyperglycemia by 12 weeks of age with a corresponding decrease in insulin levels. Pancreatic beta cells develop
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| 006373 | 129-Braftm1Sva/J | Repository- Live |
| Homozygous "floxed B-raf" (B-raff/f) mice are viable and fertile with normal B-raf protein expression. When bred to mice expressing Cre recombinase under the control of a promoter of interest, exon 12 of the targeted gene is deleted in the tissue of interest. These mutant mice may be useful in neurological studies such as Ras/Raf and MEK/ERK signaling, synaptic (neural) plasticity, learning and memory. For example, when crossed to a strain expressing Cre recombinase in nervous tissue (see Stock No. 003771), this mutant mouse strain may be useful in studies of neuron development. For example, when crossed to a strain expressing interferon inducible Cre recombinase (see Stock No. 003755), this mutant mouse strain may be useful in studies of extraembryonic mammmalian development. | ||
| 007965 | 129S-Dvl1tm1Awb/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of MEF (mouse embryonic fibroblasts) derived from homozygotes. Homozygotes exhibit diminished social interaction behavior, do not barber or trim whiskers of cagemates, show subordinance in social dominance tests, do not sleep huddled together and do not build nests. Although mutants have an attenuated prepulse inhibition of acoustic and tactile startle (sensorimotor gating of the startle reflex), they do not exhibit any deficits in locomotor or cognitive function. This mutant mouse strain may be useful in studies of social behavior, sensorimotor gating, and possibly psychiatric disorders. | ||
| 001673 | AXB1/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001681 | AXB10/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001683 | AXB12/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001826 | AXB13/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB13/PgnJ and AXB14/PgnJ are considered ?sister strains? being identical throughout much of the genome but differing in large regions of Chromosomes 11, 12, 13, and in small regions of a few other Chromosomes. Because these two strains are "near congenics" a nomenclature change has been made to update AXB14/PgnJ to AXB13a/PgnJ. In general, 'sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a ?near congenic? for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their suscepti
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| 001685 | AXB15/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001687 | AXB19/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB18/Pgn, AXB19/Pgn, and AXB20/Pgn were found to be highly similar in their overall genomes, but with particular Chromosomes differing between them. Two of these "sister" strains were renamed. AXB19/Pgn was designated the primary strain since it has the best traceable history, and therefore its name remained unchanged. AXB18/Pgn was renamed AXB19a/Pgn and AXB20/Pgn was renamed AXB19b/Pgn. In general, the "sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a "near congenic" for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalu ..... For more information please see the full descriiption on the strain data sheet | ||
| 001686 | AXB19a/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB18/Pgn, AXB19/Pgn, and AXB20/Pgn were found to be highly similar in their overall genomes, but with particular Chromosomes differing between them. Two of these "sister" strains were renamed. AXB19/Pgn was designated the primary strain since it has the best traceable history, and therefore its name remained unchanged. AXB18/Pgn was renamed AXB19a/Pgn and AXB20/Pgn was renamed AXB19b/Pgn. In general, the "sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a "near congenic" for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalu ..... For more information please see the full descriiption on the strain data sheet | ||
| 001688 | AXB19b/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. AXB18/Pgn, AXB19/Pgn, and AXB20/Pgn were found to be highly similar in their overall genomes, but with particular Chromosomes differing between them. Two of these "sister" strains were renamed. AXB19/Pgn was designated the primary strain since it has the best traceable history, and therefore its name remained unchanged. AXB18/Pgn was renamed AXB19a/Pgn and AXB20/Pgn was renamed AXB19b/Pgn. In general, the "sister" strains (those with suffixes of a or b) should not be used for primary screening/QTL mapping. However, if a QTL is located in a region of difference in a sister recombinant inbred then this strain can serve as a "near congenic" for additional analysis. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalu ..... For more information please see the full descriiption on the strain data sheet | ||
| 001674 | AXB2/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001690 | AXB23/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001691 | AXB24/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001676 | AXB4/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001677 | AXB5/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001678 | AXB6/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 001679 | AXB8/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form | ||
| 006963 | B6(101)-Mdh1am1H/LvtJ | Repository- Live |
| Homozygotes die at approximately embryonic day 17.5 (E17.5), but heterozygotes are viable and fertile. Homozygous embryos are nearly colorless, are approximately half the size of heterozygous and wildtype littermates, and show altered or delayed brain/body development. There may be a vascular defect. Decreased expression of this gene has previously been implicated with cases of schizophrenia. | ||
| 008149 | B6(Cg)-Snord116tm1.1Uta/J | Repository- Live |
| Mice homozygous for this Snord116del (1-loxP or knockout) allele are viable and fertile. As the Snord116 gene cluster is imprinted and expressed only from the paternal allele, mice with paternal inheritance of the deletion lack expression of the targeted Snord116 small nucleolar RNAs (snoRNAs) gene cluster in brain tissues. Similarly, paternal transmission of the mutant allele is required to obtain the mutant phenotype in offspring. Affected heterozygotes (paternal deleted/maternal wildtype) recapitulate a subset of Prader-Willi syndrome (PWS) characteristics, including early-onset postnatal growth retardation, delayed sexual maturation, increased anxiety, motor learning deficit and hyperphagia (but not obesity). Other reported abnormalities include altered metabolic fuel usage, prolonged meal time, and increased levels of circulating ghrelin. These Snord116del mice may be useful in studying growth and feeding regulation, mechanisms of obesity, and pa
..... For more information please see the full descriiption on the strain data sheet | ||
| 006257 | B6.129-Aldh5a1tm1Kmg/J | Repository- Live |
| Homozygous mutation of this gene results in reduced body weight, ataxia, seizures, gliosis of the hippocampus, and eventual status epilepticus. From 19-26 days of age, repetitive tonic-clonic seizures results in more than 95% mortality. Biochemical assays shows complete ablation of the endogenous enzymatic activity in the brains, livers, hearts, and kidneys of homozygous mutant mice. Homozygotes have increased levels of GHB and GABA in liver and brain tissues, as well as in urine. Phenotype can be rescued to varying degrees utilizing a number of both pharmacotherapeutic and gene therapeutic approaches. Although heterozygous mice have approximately 50% of the endogenous enzyme activity compared to wildtype mice, they are viable and fertile. Mice with this targeted mutation may be useful in studying succinate semialdehyde dehydrogenase (SSADH) deficiency and to explore the effect of GABA and GHB accumulation on central nervous system development and function. | ||
| 006874 | B6.129-Gabra4tm1.2Geh/J | Repository- Live |
| Mice homozygous for this GABAA-R alpha4F allele are viable and fertile. These mutant mice have loxP sites flanking exon 3 of the targeted gene. When bred to Cre-recombinase expressing mice, offspring will have a deletion of exon 3 in the cre expressing tissue(s). These "floxed" mice may be useful in neurological studies including behavior and neurotransmitter function. Of note, several strains bearing gamma-aminobutyric acid (GABA-A) receptor mutations are available from this donating investigator (Dr. Gregg Homanics, University of Pittsburgh), including Gabra1 (Stock No. 004318), Gabra4 (Stock No. 006874), Gabra6 (Stock No. 002710), Gabrb3 (Stock No. 002711), Gabrd (Stock No.
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| 007708 | B6.129-Gt(ROSA)26Sortm1(HD*103Q)Xwy/J | Repository- Live |
| Mice heterozygous for the RosaHD mutant allele are viable and fertile. These mice have the neuropathogenic polyQ-mutant variant of the human Huntingtin protein (mhtt-exon1; 103Q) inserted into the Gt(ROSA)26Sor locus. Expression of mhtt-exon1 is blocked by an upstream loxP-flanked transcriptional STOP sequence. When bred to mice with a Cre recombinase gene under the control of a promoter of interest, the STOP sequence is deleted in the tissue of interest, and mhtt-exon1 expression is observed. As these RosaHD mutant mice allow cre-conditional expression of the neuropathogenic mhtt-exon1 protein, they may be useful in studying Huntington's disease (HD) or other polyQ disorders. Of note, sequencing of the polyQ region (using mice from the 11th backcross) indicate the actual number of repeats to be 98. For example, when bred to strains expressing cre in brain tissues (such as Nestin-Cre (see Stock No. 003771
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| 008320 | B6.129-Leprtm2(cre)Rck/J | Repository- Live |
| Mice hemizygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. Cre activity is demonstrable in the hypothalmus (arcuate, dorsomedial (DMH), lateral (LH), and ventromedial (VMH) nuclei), limbic and cortical brain regions (basolateral amygdaloid nucleus (BLA), piriform cortex (Pir), and lateral entorhinal cortex (LEnt)), and retrosplenial cortex. When bred with a mouse containing a loxP site-flanked sequence of interest, Cre-mediated recombination results in deletion of the flanked genome in tissues that normally express the gene. This strain has been used in virus-assisted mapping of neural inputs and may be useful in studies of neural features of feeding behaviors. | ||
| 008233 | B6.129-Nrgntm1Kph/J | Repository- Live |
| Homozygous neurogranin-deficient (Ng-/-) mice are viable and fertile (although the donating investigator reports that homozygous females do not nurse their pups as well as wildtype or heterozygous mothers). Homozygotes have no mRNA or protein from the targeted gene observed in brain tissues. Expression of lacZ is observed in a manner consistent with the endogenous gene. Ng-/- mice exhibit impaired spatial learning, altered hippocampal short- and long-term plasticity (including long-term potentiation induction), and decreased activated CaMKII. Heterozygotes show similar, yet milder, effects. These neurogranin- (Ng or RC3)-mutant mice may be useful for neurological studies involving memory and learning, neuronal signaling pathways (including calmodulin, alpha-CaMKII, protein kinase A, protein kinase C, MAPK, and CREB), attention deficit-hyperactivity disorder (ADHD), and schizophrenia. | ||
| 004146 | B6.129-Tg(Pcp2-cre)2Mpin/J | Repository- Live |
| These transgenic mice express a cre gene inserted into exon 4 of a Pcp2 gene. Mice homozygous for the insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Recombinase activity is observed in most Purkinje cells and some retinal bipolar neurons. Small amounts of activity are observed in an unidentified population of cells of the central nervous system tissue. Recombination is first observed around postnatal day 6 and is fully established 2 to 3 weeks after birth. | ||
| 007566 | B6.129P2-Clip2tm1.1Gal/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and fertile. Female homozygotes adults have lower body weights and smaller body length when compared to wildtype. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brain tissue. A splice acceptor site introduced into the lacZ reporter cassette results in a hybrid Clip2-lacZ transcript. Beta galactosidase staining is observed primarily in the hippocampus and in other areas of the brain. Homozygotes exhibit a mild growth retardation. The average copus callosum volume is significantly smaller than wildtype. Homozygotes and heterozygotes exhibit abnormal behavior indicative of hippocampal defects. In contextual fear-conditioning tests, mutant mice have a diminished response, although in cued fear-conditioning tests mutant mice exhibit normal behavior. Synaptic plasticity in the CA1 area of the hippocampus is decreased in mutant mice. Both heterozygotes and homozygotes e
..... For more information please see the full descriiption on the strain data sheet | ||
| 007808 | B6.129P2-Grin3btm1Yaha/J | Repository- Live |
| Mice homozygous for this NR3B (Grin3b) mutant allele are viable and fertile, with no RNA from the targeted allele expressed in adult spinal cord. Homozygotes show a moderate but significant impairment in motor learning or coordination, decreased body weight with age, and decreased activity in their home cages. In addition, homozygous mice exhibit highly increased social interactions with their familiar cage mates in their home cage, with moderately increased anxiety-like behavior and decreased social interaction in novel environments. These NR3B (Grin3b) mutant mice may be useful in neurobiological studies; specifically studies involving NMDA receptor and NR3B function in cranial and spinal somatic motor neurons. | ||
| 005439 | B6.129S-Mecp2tm1Hzo/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and fertile. A truncated gene product (protein) is detected by immunohistochemical analysis of brain tissue. By 6 weeks of age, male mutant mice begin to exhibit tremors, progressive motor dysfunction, oily disheveled fur, hypoactivity, myoclonic seizures, and kyphosis. Approximately 10% of male mutants die between 10 and 12 months of age. Heterozygous female mice exhibit a milder phenotype. All mutant male mice and 62% of female heterozygotes exhibit a repetitive clasping movement of their forelimbs and exhibit tremors. The Donating Investigator reports that the myoclonic seizures, kyphosis and reduced survival were observed in aged male mutants on a 129/SvEv genetic background. This mutant mouse strain may be useful in studies of Rett Syndrome. The Howard Hughes Medical Institute and the National Institutes of Health supported the creation of this model. Importation of this model was supported by the Rett Syndrome Rese
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| 007557 | B6.129S2-Oprd1tm1Kff/J | Repository- Live |
| Mice homozygous for this delta-opioid receptor mutant allele (DOR-) are viable and fertile. DOR-selective ligand binding is absent in vitro on brain membranes from homozygous mice. Unlike mutant mice deficient in kappa- or mu-opioid receptors (Stock No. 007558 or 007559, respectively), homozygous DOR- mutants exhibit increased anxiety and depressive-like behavior but no alteration of spontaneous pain perception. Homozygous DOR- mice also have increased ethanol self-administration and increased inflammatory pain. These DOR mutant mice may be useful in studying the biological activity of opioids andanalgesics, mechanical nociception, inflammatory pain, and emotional disorders.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first ch
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| 007558 | B6.129S2-Oprk1tm1Kff/J | Repository- Live |
| Mice homozygous for this kappa-opioid receptor mutant allele (KOR-) are viable and fertile. KOR-selective ligand binding is absent on brain membranes from homozygous mice. In contrast to mutant mice deficient of delta- or mu-opioid receptors (Stock No. 007557 or 007559), KOR- homozygotes have normal mechanical pain thresholds, but greatly increased sensitivity to chemical visceral pain. KOR- homozygotes also exhibit normal spontaneous stress responses (unlike delta-opioid receptor null mice). Homozygous KOR- mice also show decreased ethanol self-administration and decreased THC-conditioned place aversion. These KOR mutant mice may be useful in studying biological activity of opioids, analgesics, spinally mediated thermal nociception and chemical visceral pain thresholds. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. These mut
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| 007559 | B6.129S2-Oprm1tm1Kff/J | Repository- Live |
| Mice homozygous for this mu-opioid receptor mutant allele (MOR-) are viable and fertile. MOR-selective ligand binding is absent on brain membranes from homozygous mice. Homozygous MOR- mice exhibit a lack of morphine analgesia, reward, and withdrawal. This is accompanied by decreased mechanical, thermal, and chemical pain thresholds. Homozygous MOR- mice also show decreased ethanol self-administration and decreased THC-conditioned place aversion. In contrast to mutant mice deficient of delta- or kappa-opioid receptors (Stock No. 007557 or 007558, respectively), MOR- homozygotes exhibit hypolocomotive spontaneous stress responses. Indeed, the reduced anxiety and depressive-like behavior observed in MOR- mutants is in stark contrast to kappa-opioid receptor deficient mice. These MOR mutant mice may be useful in studying the biological activity of opioids, analgesics, and responses to mechanical, chemical and thermal nociception at a supraspinal level. In an attempt to offer alleles
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| 008123 | B6.129S4(129S6)-Sstr3tm1Ute/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern blot, in situ hybridization or radioimmunoassay analysis of brain tissue. Mutants have severely impaired spatial learning memory. Non-selective somatostatin ligand binding assays of the brain reveal a significant decrease in binding in the olfactory bulb with an increase in binding in the deep layer of the piriform cortex, the striatum, the hippocampus, the substantia nigra and the locus coeruleus. This mutant mouse strain may be useful in studies of learning and memory and endocrinology. | ||
| 008124 | B6.129S4(129S6)-Sstr4tm1Ute/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, and normal in size. Homozygotes have unprovoked seizures. Non-selective somatostatin ligand binding assays of the brain reveal a significant decrease in binding in the olfactory bulb and hippocampus CA1 field. Of note, this targeted gene is on Chromosome 2 near agouti, although these mice have been backcrossed for more than 10 generations onto C57BL/6NHsd they are agouti. This mutant mouse strain may be useful in studies of learning and memory, epilepsy and endocrinology. | ||
| 005246 | B6.129S4-Grin1tm2Stl/J | Repository- Live |
| These mice possess loxP sites flanking approximately 12kb of sequence of the targeted gene that encodes the entire transmembrane domain and C-terminal region. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to a strain expressing Cre recombinase in the CA3 region of the hippocampus (see Stock No. 006474 for example), this mutant mouse strain may be useful in studies of associative memory recall. When bred to a strain expressing Cre recombinase in the CA1 region of the hippocampus (see Stock No. 005359 for example), this mutant mouse strain may be useful in studies of nonspacial memory. | ||
| 007969 | B6.129S6-Dvl1tm1Awb/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of MEF (mouse embryonic fibroblasts) derived from homozygotes. Homozygotes exhibit diminished social interaction behavior, do not barber or trim whiskers of cagemates, show subordinance in social dominance tests, do not sleep huddled together and do not build nests. Although mutants have an attenuated prepulse inhibition of acoustic and tactile startle (sensorimotor gating of the startle reflex), they do not exhibit any deficits in locomotor or cognitive function. This mutant mouse strain may be useful in studies of social behavior, sensorimotor gating, and possibly psychiatric disorders.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele wa
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| 003819 | B6.129S7-Per2tm1Brd/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display gross physical or behavioral abnormalities. A mutant transcript, if translated, would generate a protein with an 87 amino acid deletion. When maintained in constant darkness, two phenotypic components are exhibited: a shortened circadian period and a loss of persistent circadian rhythmicity. When housed under constant light, homozygotes exhibit normal activity rhythm but a period length of less than 24 hours. Female homozygotes, 9-12 months of age, exhibit low reproductive success and produce small litters when compared to wildtype. This mutant mouse strain may be useful in studies related to the regulation of the sleep-wake cycle. | ||
| 006606 | B6.129X1-Camkk1tm1Tch/J | Repository- Live |
| Homozygotes are viable and fertile. Immunoblots using antibodies against both carboxy- and amino-terminal peptide sequences confirms the absence of wildtype protein in brain tissue. These CaMKKalpha-deficient mice exhibit deficits in context fear during both conditioning and long-term follow-up testing. This is accompanied by impaired activation of other kinases and substrates downstream in the Ca2+/calmodulin kinase (CaMK) cascade. Homozygous mice have normal long-term spatial memory formation, cued fear conditioning, long-term potentiation and anxiety-like behavior levels. These mutant mice may be useful in neurological studies involving the CaMK cascade, neuronal gene transcription, synaptic plasticity, contextual fear and long-term memory consolidation. | ||
| 006562 | B6.CBy(Cg)-Gusbmps Gpi1a-m1J/BrkJ | Repository- Live |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They may be useful in developing new therapies (enzyme replacement, cell transplantation, gene therapy) broadly applicable to other lysosomal storage diseases. | ||
| 004103 | B6.Cg-Tac1tm1Bbm/J | Repository- Live |
| Mice that are homozygous null for the Tac1 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Tac1 protein products (substance P or neurokinin A) are not immunodetectable. These mice have significantly reduced nociceptive pain responses to moderate to intense stimuli. Neurogenic inflammation is absent. Mutant mice are resistant to kainate-induced seizures and neurotoxicity. These mice provide a useful tool for studying the contribution of tachykinin peptides to pain processing and inflammatory disease states. | ||
| 005866 | B6.Cg-Tg(APP695)3Dbo Tg(PSEN1dE9)S9Dbo/J | Repository- Live |
| Double transgenic mice are viable and fertile. At 6 months of age, double-transgenic mice show visible amyloid plaque deposition but are indistinguishable from nontransgenic animals in all cognitive measures. By 18 months, amyloid deposits were much higher in APPswe/PS1dE9 mice with statistically significant but mild decreases in cholinergic markers (cortex and hippocampus) and somatostatin levels (cortex). Performance of older double-transgenic mice is impaired in all cognitive tasks, and deficits in episodic-like memory tasks correlate with total amyloid-beta peptide loads in the brain. | ||
| 005864 | B6.Cg-Tg(APPswe,PSEN1dE9)85Dbo/J | Repository- Live |
| Double transgenic mice express a chimeric mouse/human amyloid precursor protein (Mo/HuAPP695swe) and a mutant human presenilin 1 (PS1-dE9) both directed to CNS neurons. Both mutations are associated with early-onset Alzheimer's disease. The “humanized” Mo/HuAPP695swe transgene allows the mice to secrete a human A-beta peptide. Both the transgenic peptide and holoprotein can be detected by antibodies specific for human sequence within this region (Signet Laboratories' monoclonal 6E10 antibody). The included Swedish mutations (K595N/M596L) elevate the amount of A-beta produced from the transgene by favoring processing through the beta-secretase pathway. This “humanized” Mo/HuAPP695swe protein is immunodetected in whole brain protein homogenates. The transgenic mutant human presenilin protein (PS1-dE9), which in high levels displaces detectable endogenous mouse protein, is also immunodetected in whole brain protein homogenates. The donating investigator reports tra
..... For more information please see the full descriiption on the strain data sheet | ||
| 007574 | B6.Cg-Tg(Camk2a-Crebbp*)1364Tabe/J | Repository- Live |
| Mice hemizygous for this "CaMKIIα-FLAG-CBPΔ1" transgene are viable and fertile. Expression of this FLAG-epitope tagged, dominant negative truncation of the CREB-binding protein (FLAG-CBPΔ1) is spatially directed to neurons in the forebrain (hippocampus, amygdala, striatum, and cortex) and temporally directed to postnatal development by the CaMKIIα promoter. This dominant negative mutant form of CBP (designed to interrupt transcription factors utilizing CBP as a coactivator for the expression of their target genes) is expressed from the transgene at 95% of endogenous CBP levels in the hippocampus and 84% of endogenous CBP levels in the cortex. Hemizygous mice exhibit hippocampus-dependent memory deficits (such as reduced long-term potentiation, defective spatial learning, and impaired contextual fear conditioning) with none of the developmental impairments observed in CBP-deficient mutant models. These CaMKIIα-FLAG-CBPΔ1 transgenic mice may be useful
..... For more information please see the full descriiption on the strain data sheet | ||
| 007004 | B6.Cg-Tg(Camk2a-tTA)1Mmay/DboJ | Repository- Live |
| Transgenic mice expressing the tetracycline-controlled transactivator protein (tTA) under regulatory control of the forebrain-specific calcium-calmodulin-dependent kinase II (Camk2a) promoter are viable and fertile. When hemizygotes are mated to a second strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene can be blocked by administration of the tetracycline analog, doxycycline (dox). These mice are a "Tet-Off" tool that allow the inducible expression of genes in forebrain neurons, and may be useful in studying brain disorders such as Alzheimer's disease (when used in conjunction with Stock No. 005706, Stock No. 007049, Stock No. 007051, Stock No. 007052), Parkinson's
..... For more information please see the full descriiption on the strain data sheet | ||
| 006471 | B6.Cg-Tg(HDexon1)61Gpb/J | Repository- Live |
| Mice have been generated that are transgenic for the 5' end of the human HD gene carrying (CAG)115-(CAG)150 repeat expansions. In this founder line (61Gpb), as well as another similar line (62Gpb, see Stock No. 006494), the transgene is ubiquitously expressed. Transgenic mice exhibit a progressive neurological phenotype that mimics many of the features of HD, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures, as well as nonmovement disorder components, including unusual vocalization. They urinate frequently and exhibit loss of body weight and muscle bulk through the course of the disease. Neurologically they develop Neuronal Intranuclear Inclusions (NII) which contain both the huntingtin and ubiquitin proteins. These NII have also been identified in human HD patients. The age of onset of HD symptoms is reported to occur between 15 and 21 weeks for this 61Gpb line. These HDexon1
..... For more information please see the full descriiption on the strain data sheet | ||
| 008323 | B6.Cg-Tg(Mc4r-MAPT/GFP*)21Rck/J | Repository- Live |
| These mice express a tau (MAPT)-sapphire green fluorescent protein (GFP) under the transcriptional control of the mouse melanocortin 4 receptor (Mc4r) promoter. Central nervous system distribution of GFP-producing cells is identical to that of Mc4r mRNA in wild-type mice and nearly all GFP-producing cells coexpress melanocortin 4 mRNA. This strain may be useful in studying the role of melanocortin signaling in the regulation of feeding behavior and autonomic homeostasis. Hemizygotes are viable and fertile and do not display any gross physical or behavioral abnormalities. | ||
| 008321 | B6.Cg-Tg(Npy-MAPT/GFP*)1Rck/J | Repository- Live |
| These mice express a tau (MAPT)-sapphire green fluorescent protein (GFP) under the transcriptional control of the mouse neuropeptide Y (Npy) promoter. Immunohistochemistry for NPY in colchicine-treated animals demonstrated ~95% colocalization of NPY with the GFP-expressing neurons in the hypothalamic arcuate nucleus. This strain has been useful in studying the role of neuropeptide Y and leptin in food intake. Hemizygotes are viable and fertile and do not display any gross physical or behavioral abnormalities. | ||
| 006293 | B6.Cg-Tg(PDGFB-APPSwInd)20Lms/2J | Repository- Live |
| These transgenic mice express a mutant form of the human amyloid protein precursor bearing both the Swedish (K670N/M671L) and the Indiana (V717F) mutations (APPSwInd). Expression of the transgenic insert is directed by the human platelet-derived growth factor beta polypeptide (PDGFB) promoter. Hemizygotes express immunodetectable transgene product in cerebral neurons, with the highest level of expression occurring in the neocortex and hippocampus. Enzyme-linked immunosorbent assay (ELISA) analysis reveals approximate total amyloid beta peptides and 42 amino acid length amyloid beta peptides in neocortical and hippocampal tissue from mutant mice. At five to seven months of age diffuse amyloid beta peptides deposition in the dendate gyrus and neocortex forms. Amyloid deposition is progressive with all transgenic mice exhibiting plaques by age eight to 10 months. This mutant mouse strain represents a model that may be useful in studies of the pathogenesis of Familial Alzheim
..... For more information please see the full descriiption on the strain data sheet | ||
| 008322 | B6.Cg-Tg(Pomc-MAPT/GFP*)1Rck/J | Repository- Live |
| These mice express a tau (MAPT)-sapphire green fluorescent protein (GFP) under the transcriptional control of the mouse pro-opiomelanocortin-alpha (Pomc) promoter. Immunohistochemistry for POMC in colchicine-treated animals demonstrated greater than 99% colocalization of POMC with the GFP-expressing neurons in the hypothalamic arcuate nucleus. This strain has been useful in studying the role of Pomc and leptin in food intake and may be useful in further understanding the function of the associated neurons. Hemizygotes are viable and fertile and do not display any gross physical or behavioral abnormalities. | ||
| 008277 | B6.Cg-Tg(tetO-Clockm1Jt)CL57Jt/J | Repository- Live |
| Homozygous transgenic mice are viable and fertile. These animals express the Clockdelta19 mutation under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoters, transgene expression can be conditionally regulated in the appropriate tissue of the bitransgenic offspring with the tetracycline analog, doxycycline.
Transgenic expression of the Clock gene in the suprachiasmatic nucleus and brain of mice regulates the period length of circadian locomotor rhythms. This dominant negative mutant transgene lengthens the period of circadian locomotor rhythms in mice, whereas overexpression of the wild-type transgene (Stock No. 008278) shortens the period. These effect
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| 002711 | B6;129-Gabrb3tm1Geh/J | Repository- Live |
| The gamma-Aminobutyric acid type A receptors mediate the majority of rapid inhibitory synaptic transmission in the CNS. The beta3 subunit is an essential component of these receptors in many brain regions, especially during development, and is implicated in several pathophysiologic processes. The majority of mice homozygous for the Gabrb3tm1Geh mutation (or beta3-/-) die at birth with ~60% displaying cleft palate and the remaining ~35% die for unidentified reasons. Homozygous females that survive are fertile but do not care for their pups. Survivors have frequent myoclonus and occasional epileptic seizures, are hypersensitive to external stimuli and handling, have a lack of coordination and display altered responses to certain anesthesias. In addition, the observed behavioral deficits (especially regarding social behaviors) indicate that mutant mice may be a useful model of autism spectrum disorders. Of note, several strains bearing gamma-aminobutyric acid (GABA-A)
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| 005034 | B6;129-Hcn1tm2Kndl/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No mRNA encoding the pore/S6 transmembrane domain is detected by in situ hybridization. No HCN1 protein is detected by Western blot analysis of membrane extracts from cerebellum, hippocampus or cortex. Mutant mice exhibit impaired learning capacity in visible platform swimming water maze task and rotorod test, and abnormal eye blink conditioning response. Purkinje cell electrophysiology is abnormal. This mutant mouse strain may be useful in studies of learning, memory and neurophysiology. | ||
| 007605 | B6;129P-Psen1tm1Vln/J | Repository- Live |
| These mice possess loxP sites on either side of exon 7 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these "floxed" mice are bred to mice that express Cre recombinase, resulting offspring can have one of three resulting genotypes (only exon 7 deleted, only the neo selection cassette deleted, or both exon 7 and the neo selection cassette deleted) in the cre-expressing tissue(s). These PS1-floxed mice may be useful in generating conditional knockouts of Presenilin 1 for studying Alzheimer's Disease. | ||
| 006401 | B6;129P-Trpa1tm1Kykw/J | Repository- Live |
| Homozygous mice are viable and fertile. The donating investigator reports a dramatic loss of fecundity after 5-6 months of age. The targeting vector contains an endoplasmic reticulum (ER) retention signal (KDEL), which is reported to sequester the potential truncated mRNA product in the ER. The vector also contains an IRES-PLAP reporter gene, allowing extracellular antibody staining/chromogenic development tracking of cells normally expressing the endogenous gene. Homozygous mice display behavioral deficits in response to mustard oil, cold, and punctate mechanical stimuli. These mice have a normal startle reflex to loud noise, a normal sense of balance, a normal auditory brainstem response, and normal transduction currents in vestibular hair cells. These mutants may be useful in neurobiological studies involving dorsal root ganglion neurons and cells of the inner ear, as well as for auditory, temperature, or chemical irritant trials. | ||
| 006849 | B6;129P2-Mecp2tm2Bird/J | Repository- Live |
| These mice possess a loxP-flanked STOP cassette in intron 2 of the targeted gene on the X chromosome. Western blot and hybridization analysis confirm the absence of wildtype protein from the targeted allele. Hemizygous (Mecp2lox-Stop/y) males do not breed and develop Rett syndrome symptoms (reduced mobility, hindlimb clasping) at approximately 6 weeks of age, with death occurring at approximately 11 weeks of age. Heterozygous females are fertile until developing Rett syndrome characteristics at 4-12 months of age. This Rett syndrome-like phenotype is similar to that observed for the traditional knock-out allele (see Stock No. 003890). Cre recombinase-mediated removal of the floxed-STOP cassette restores transcription from the targeted allele and MECP2 protein activity to normal, and reverses the Rett syndrome-like neurological defects. This mutant mouse strain may be bred to a strain expressing tamoxi
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| 002466 | B6;129P2-Prkcctm1Stl/J | Repository- Live |
| Mice homozygous for the Prkcctm1Stl targeted mutation are viable and develop normally. Homozygous mice show diminished long-term potentiation (LTP) in the hippocampus, but two other types of synaptic plasticities are normal, namely long-term depression and paired-pulse facilitation. Despite this diminished LTP capacity homozygotes can learn to do hippocampus-dependant tasks, such as the Morris water maze and context-dependent fear conditioning, with only slight deficits. | ||
| 006410 | B6;129S6-Chattm1(cre)Lowl/J | Repository- Live |
| Homozygous mice maintained at The Jackson Laboratory are viable and fertile. An "IRES-Cre" sequence is inserted downstream of the stop codon such that cre expression is controlled by the endogenous Chat gene promoter. Chat gene expression, however, is unaffected. Cre recombinase activity is reported in all cholinergic neurons. These mice may be useful for "Cre-lox" technology applications in neurobiology, including studies of motor function, learning and memory, Alzheimer's disease, and Down syndrome, and in obesity and diabetes research. | ||
| 002385 | B6;129S7-Fyntm1Sor/J | Repository- Live |
| Mice homozygous for the Fyntm1Sor targeted mutation are viable and fertile displaying no overt phenotype. T cell receptor signaling is defective in homozygous mutant mice and are characterized by a reduction in levels of tyrosine-phosphorylated proteins, failure to flux calcium in response to TCR cross-linking, and a reduction in production of calcium-related IL2. THY-1-induced proliferation is also reduced in thymocytes but not in splenic T cells. Neurological defects include blunted long-term potentiation (LTP), impaired special learning, and altered hippocampal development. | ||
| 003692 | B6;129X1-Sncatm1Rosl/J | Repository- Live |
| Homozygous null mice are viable, fertile, normal in size and do not display any gross abnormalities. No gene product (mRNA or protein) is detected in brain tissue. A wild-type complement of dopamine neurons, fibers and synaptic terminals is present and the overall brain architecture appears to be intact. They suffer from a reduction in total striatal dopamine and exhibit an attenuated locomotor response when given amphetamine. Normal dopamine release is observed upon stimulation of the nigrostriatal terminal with a single electrical pulse. When multiple stimuli are applied however, null mice exhibit an accelerated recovery of dopamine release. A similar acceleration is seen in wildtype mice in the presence of increased extracellular calcium. The phenotype observed in homozygous Snca-null mice suggests that Snca is an activity-dependent negative regulator of dopamine neurotransmission. | ||
| 006302 | B6;SJL-Slc6a3tm1.1(cre)Bkmn/J | Repository- Live |
| Mice homozygous for this dopamine transporter IRES-cre (DATIREScre or DAT-cre) mutant allele are viable and fertile. Cre recombinase activity is observed as early as embryonic day 15, and co-localizes with endogenous gene expression in adult dopaminergic cell groups (substantia nigra (SN) and ventral tegmental area (VTA), as well as in the retrorubral field). Lower Cre recombinase activity is detected in adult olfactory bulb glomeruli, mimicking the known lower Slc6a3 (or DAT) expression in this tissue. Although the pattern and intensity of DAT immunostaining in the SN, VTA and striatum do not differ between wildtype and mutant mice, striatum DAT protein levels are moderately reduced (17%) in heterozygotes and significantly reduced (47%) in homozygotes. This decrease in DAT protein levels in homozygous mutant striatum is associated with significantly increased neuropeptide PDyn (but not D1, D2, or PPE) mRNA levels compared to wildtype. Increases in these mRNA l
..... For more information please see the full descriiption on the strain data sheet | ||
| 003627 | B6C3-Tg(HD82Gln)81Dbo/J | Repository- Live |
| Mice expressing this transgene appear normal at birth through 1-2 months. Mice fail to gain weight, develop tremors, hypokinesis and lack coordination. They exhibit an abnormal gait and frequent hind limb clasping. Life expectancy is 5-6 months. Studies using huntingtin antibodies indicated numerous immunoreactive nuclear inclusions in multiple neuron populations. Neuritic damage is evident. | ||
| 006004 | B6C3-Tg(tetO-APPSwInd)885Dbo/J | Repository- Live |
| Hemizygous mice are viable and fertile. These transgenic mice express a chimeric mouse/human amyloid precursor protein (APP) bearing the Swedish (KM570/571NL) and Indiana (V617F) mutations associated with Alzheimer's disease (APPswe/ind) under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoters , APPswe/ind transgene expression can be regulated in the appropriate tissue of the bitransgenic offspring with the tetracycline analog, doxycycline. When bred to a strain expressing rtTA or tTA in brain tissues (see Stock No. 003010, for example), this mutant mouse strain may be useful in studies of Alzheimer's Disease. | ||
| 001924 | B6EiC3Sn a/A-Ts(1716)65Dn | Repository- Live |
| Segmentally trisomic Ts(1716)65Dn mice provide a postnatal model for Down syndrome. Ts65Dn mice have three copies of most of the genes on mouse Chr 16 that are homologues of human Chr 21 genes. These extra genes, along with the centromere and about 5% of proximal Chr 17 are contained in a small extra chromosome derived from a reciprocal translocation. Neural cognitive deficits and behavioral abnormalities have been noted in Ts65Dn mice. They have spatial learning and memory defects as assessed in the Morris water maze and the radial arm maze, show developmental delay in sensorimotor milestones, and exhibit locomotor hyperactivity, lack of behavioral inhibition, and stereotypic behavior. They perform similar to controls in visual placing, balance, prehensile reflex and traction on a horizontal bar, motor coordination, swimming ability, olfaction orienting. They also show altered noradrenergic transmission in the hippocampus and cerebral cortex and degeneration of basal forebr
..... For more information please see the full descriiption on the strain data sheet | ||
| 001692 | BXA1/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin.The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001699 | BXA11/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001700 | BXA12/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001701 | BXA13/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001702 | BXA14/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. In 2004 a phenotype of small body size was found to be segregating in this colony after recovery from cryopreservation. It appears that this phenotype is segregating recessively in this strain and is present in the cryopreserved bank stock. The expressed phenotype is small size relative to littermates and mice with this diminished body size often catch up to their littermantes in body size af ..... For more information please see the full descriiption on the strain data sheet | ||
| 001703 | BXA16/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001693 | BXA2/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001710 | BXA24/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001711 | BXA25/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001999 | BXA26/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001694 | BXA4/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001696 | BXA7/PgnJ | Repository- Live |
| The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 001697 | BXA8/PgnJ | Repository- Live |
| Through high density SNP analysis, some AXB and BXA recombinant inbred strains were shown to be the same or nearly the same genetically. BXA17/Pgn was found to be a replica of BXA8/Pgn. BXA17/Pgn was lost in 1989 or 1990. The AXB and BXA set of RI strains are useful in the genetic analysis of several complex diseases including cardiovascular disease, diabetes, cancer, cleft palate, and hydrocephalus. The individual strains within the RI set also differ in their susceptibility to infectious diseases and in their responses to alcohol, stress, and endotoxin. The strain distribution pattern (SDP) for both the AXB and BXA RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000036 | BXD1/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity.The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000012 | BXD11/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000045 | BXD12/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000040 | BXD13/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000329 | BXD14/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000095 | BXD15/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000013 | BXD16/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. A mutation has been identified in the BXD16 strain in the amylase 1 gene from the parental Amy1a allele to an allele that has an electrophoretic mobility closer to that of Amy1b. This allele is distinct from all others identified and no evidence of genetic contamination was found. Thus, this is believed to have resulted from a spontaneous mutation. (Hjorth, 1982.) | ||
| 000015 | BXD18/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000010 | BXD19/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000075 | BXD2/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form.
The BXD2/TyJ strain develops spontaneous arthritis in 50% of females by 8 months of age and 90% of males greater than 12 months of age. The progressive, age-related arthritis includes extensive synovial hyperplasia and marginal invasion of the metatarsophalangeal, forelimb and hindlimb joints. Adult mice exhibit glomerulonephritis, proteinuria (by 6 months), splenomegaly, and autoantibody production. (Mountz JD, et
..... | ||
| 000330 | BXD20/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity.The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000077 | BXD21/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000043 | BXD22/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 005243 | BXD24a/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000031 | BXD24b/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000041 | BXD27/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000047 | BXD28/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000029 | BXD29/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000083 | BXD31/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000078 | BXD32/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 003222 | BXD33/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 003223 | BXD34/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 003225 | BXD36/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 003227 | BXD38/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 003228 | BXD39/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 003229 | BXD40/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 003230 | BXD42/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000037 | BXD5/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000007 | BXD6/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000084 | BXD8/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity.The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 000105 | BXD9/TyJ | Repository- Live |
| The BXD RI strains are used to study the genetics of behavioral phenotypes including alcohol and drug addiction, stress, and locomotor activity. The BXD set of RI strains also are used in the genetic analysis of numerous complex or potentially complex physiologic phenotypes including differences in organ weight and bone mineral density. The strain distribution pattern (SDP) for BXD RI strains is available through the Mouse Genome Informatics Recombinant Inbred Strain Distribution Patterns Query Form. | ||
| 006581 | C57BL/6-Ppp3r1tm1Stl/J | Repository- Live |
| Mice homozygous for this "fCNB1" mutant allele are viable and fertile with no reported neurological abnormalities. These mutant mice have loxP sites flanking exons 2-4 of the endogenous gene. When bred to transgenic mice expressing Cre recombinase, exons 2-4 are deleted in the resulting offspring in only those tissues expressing cre. For example, when crossed with transgenic mice expressing Cre recombinase specifically in the forebrain (similar to Stock No. 005359), the resulting offspring show abnormalities that are strikingly similar to those described for schizophrenia. These "floxed" mice may be useful in studies of calcineurin function in T cells (via NFAT transcription of cytokine genes) and in the central nervous system in, for example, neurite extension, synaptic plasticity, learning and memory, and schizophrenia pathogenesis. | ||
| 006662 | C57BL/6-Tg(ACTB-MAP2K1*K97M)1Stl/J | Repository- Live |
| Hemizygous mice are viable and fertile. These "dnMEK1" mice express a dominant-negative mutant (K97M) form of human MEK1 (synonym: MAP2K1) following Cre-mediated removal of the upstream "Lox-STOP-Lox" cassette; when transgenic mice are bred to a cre-expressing strain, the "floxed stop" cassete is excised in the resulting offspring, and mutant MEK1 expression is observed in the cre-expressing tissue(s). In the absence of Cre recombinase, transgene expression is not detectable in the brains of these "floxed" mice Because the MEK1 mutation abolishes the protein's kinase activity but preserves its ability to interact with ERK1 and ERK2, these transgenic mice may be useful in studying MEK-dependent activation and regulation of ERK, the ERK-MAPK signaling pathway, and neurological studies involving synaptic plasticity and memory. When bred to a strain expressing Cre recombinase in the CA1 pyramidal cell layer of the hippocampus (see Stock No. For more information please see the full descriiption on the strain data sheet | ||
| 006474 | C57BL/6-Tg(Grik4-cre)G32-4Stl/J | Repository- Live |
| Mice hemizygous for this "G32-4" transgene are viable, fertile, and do not display any gross physical or behavioral abnormalities. Transgene expression (cre activity) is detectable at 14 days old in area CA3 of the hippocampus, and at 8 weeks of age, recombination is observed in nearly 100% of pyramidal cells in area CA3. Recombination is also observed in other brain areas, but at distinctly lower frequencies. If bred with mice containing a loxP-flanked sequence of interest, tissue-specific deletion of that sequence results in the offspring. Specifically, when these mice were bred with a conditional CaMKII allele (see Stock No. 006575), the resulting offspring exhibited altered neurotransmitter release. The donating investigator reports that G32-4 females may confer global Cre-mediated deletion of loxP-flanked sequences in some offspring, and recommend using male G32-4 mice exclusively for such trials. These C
..... For more information please see the full descriiption on the strain data sheet | ||
| 008278 | C57BL/6J-Tg(tetO-Clock)1Jt/J | Repository- Live |
| Homozygous transgenic mice are viable and fertile. These animals express the wildtype Clock gene under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoters, transgene expression can be conditionally regulated in the appropriate tissue of the bitransgenic offspring with the tetracycline analog, doxycycline. Transgenic expression of the Clock gene in the suprachiasmatic nucleus and brain of mice regulates the period length of circadian locomotor rhythms. This wildtype transgene shortens the period of circadian locomotor rhythms in mice, whereas overexpression of the Clockdelta19 mutant transgene (Stock No. 008277) lengthens the period. These effects
..... For more information please see the full descriiption on the strain data sheet | ||
| 007578 | CBy.Cg-Tg(HDexon1)61Gpb/J | Repository- Live |
| Mice have been generated that are transgenic for the 5' end of the human HD gene carrying approximately 100 CAG repeat expansions. In this founder line (61Gpb), the transgene is ubiquitously expressed. Transgenic mice exhibit a progressive neurological phenotype that mimics many of the features of HD, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures, as well as nonmovement disorder components, including unusual vocalization. They urinate frequently and exhibit loss of body weight and muscle bulk through the course of the disease. Neurologically they develop Neuronal Intranuclear Inclusions (NII) which contain both the huntingtin and ubiquitin proteins. These NII have also been identified in human HD patients. The age of onset of HD symptoms is reported to occur between 15 and 21 weeks for this 61Gpb line. On the BALB/cByJ genetic background, the CAG tract remains somatically stable throughout the life span of the mouse but may contr
..... For more information please see the full descriiption on the strain data sheet | ||
| 000351 | CXB1/ByJ | Repository- Live |
| Like BALB/cByJ, this recombinant inbred carries the mutation hippocampal lamination defect or Hld, an allele responsible for abnormal neuronal migration to the pyramidal cell layer (Nowakowski RS, et al, Jnl Neurogen, 1984). | ||
| 001631 | CXB10/HiAJ | Repository- Live |
| 001632 | CXB11/HiAJ | Repository- Live |
| 001633 | CXB12/HiAJ | Repository- Live |
| 001634 | CXB13/HiAJ | Repository- Live |
| 000352 | CXB2/ByJ | Repository- Live |
| 000353 | CXB3/ByJ | Repository- Live |
| Like BALB/cByJ, this recombinant inbred carries the mutation hippocampal lamination defect or Hld, an allele responsible for abnormal neuronal migration to the pyramidal cell layer (Nowakowski RS, et al, Jnl Neurogen, 1984). | ||
| 000354 | CXB4/ByJ | Repository- Live |
| Like BALB/cByJ, this recombinant inbred carries the mutation hippocampal lamination defect or Hld, an allele responsible for abnormal neuronal migration to the pyramidal cell layer (Nowakowski RS, et al, Jnl Neurogen, 1984). | ||
| 000355 | CXB5/ByJ | Repository- Live |
| Like BALB/cByJ, this recombinant inbred carries the mutation hippocampal lamination defect or Hld, an allele responsible for abnormal neuronal migration to the pyramidal cell layer (Nowakowski RS, et al, Jnl Neurogen, 1984). | ||
| 000356 | CXB6/ByJ | Repository- Live |
| 000357 | CXB7/ByJ | Repository- Live |
| The CXB7/ByJ recombinant inbred strain is widely used because of a deficiency in mu opioid receptors. Like BALB/cByJ, this recombinant inbred carries the mutation hippocampal lamination defect or Hld, an allele responsible for abnormal neuronal migration to the pyramidal cell layer (Nowakowski RS, et al, Jnl Neurogen, 1984). | ||
| 001629 | CXB8/HiAJ | Repository- Live |
| 001630 | CXB9/HiAJ | Repository- Live |
| 004938 | FVB-Tg(YAC128)53Hay/J | Repository- Live |
| These transgenic mice express the human huntingtin protein containing a 128 CAG repeat expansion. Human huntingtin mRNA and protein is detected. Hyperkinesis begins at 3 months of age with progressive motor impairment appearing at 6 months of age. This is followed by progressive neurodegeneration, starting at 9 months of age, and hypokinesis at 12 months. The motor dysfunction, Rotorod deficit, is correlated with neuronal loss. Mutants exhibit decreased brain weight and reduced striatal and cortical volumes. 18% shrinkage of striatal neurons is observed in 12 month old mutants. A significant decrease (15%) in the number of striatal neurons occurs by 12 months of age. Nuclear huntingtin aggregate inclusions of striatal neurons from 18 month old mutant mice are detected at the light microscopy level. This mutant mouse strain represents a model that may be useful in studies of Huntington's disease. | ||
| 004624 | FVB.129P2-Fmr1tm1Cgr/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and fertile. Quantitative morphological analysis of dendritic spines of visual cortex pyramidal cells reveals mutant mice have more long dendritic spines, fewer short dendritic spines and more spines with an immature morphology than wildtype littermates. These mice were backcrossed for 11 generations onto the FVB background, are homozygous for the 129P2/OlaHsd wildtype Pde6b allele and do not suffer from blindness due to retinal degeneration. This mutant mouse strain may be useful in studies related to Fragile X Syndrome. | ||
| 006143 | FVB/N-Tg(Thy1-cre)1Vln/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre activity is observed in nearly all neurons in cortex and hippocampus. When bred with any mouse containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in postnatal, neuron-specific deletion of the flanked genome. These mice may be useful in studies of the nervous system, including Alzheimer's disease. | ||
| 007247 | FVB/N-Tg(YAC353G6)W7Hay/J | Repository- Live |
| These transgenic mice express the human huntingtin protein containing a 133 CAG repeat expansion and a mutation in exon 13 conferring resistance to caspase-6 cleavage to the gene product.
Expected caspase-6 cleaved fragments are not detected in brain lysates by Western blot analysis. Transgenic mice have brain weight and striatal volume similar to wildtype controls and do not exhibit neuronal loss at 12 months of age when compared to transgenic mice that express human huntingtin protein containing a 128 CAG repeat (FVB-Tg(YAC128)53Hay/J Stock No. 004938). These transgenic mice have activity levels and motor function similar to wildtype controls, and are resistant to neuron excitotoxicity. Immunohistochemical analysis of striatal brain sections reveals delayed nuclear localization of mutant huntingtin protein in these transgenic mice at nine months of age. Between nine and 12 months of age, an increase of nuclear huntingtin is observed. Homozygotes are viable, fertile, normal in
..... For more information please see the full descriiption on the strain data sheet | ||
| 005053 | NOD.Cg-Prkdcscid Gusbmps/SndsJ | Repository- Live |
| Mice homozygous for the mps allele exhibit skeletal dysplasia as well as cognitive, hearing and visual deficits. Lifespan of the homozygotes is approximately six months. Homozygotes lack the lysomal enzyme, beta-glucoronidase, and, as a result, glycosaminoglycans accumulate in tissues throughout the body. This strain is a model for the human lysomal storage disease, mucopolysaccharidosis type VII. On the NOD-Prkdcscid background, this strain can be used for xenotransplantation experiments and cell trafficking studies (Hofling et al., 2003). | ||
| 002271 | 129-Fyntm1Sor/J | Repository-Cryopreserved |
| Mice homozygous for the Fyntm1Sor targeted mutation are viable and fertile displaying no overt phenotype. T cell receptor signaling is defective in homozygous mutant mice and are characterized by a reduction in levels of tyrosine-phosphorylated proteins, failure to flux calcium in response to TCR cross-linking, and a reduction in production of calcium-related IL2. THY-1-induced proliferation is also reduced in thymocytes but not in splenic T cells. Neurological defects include blunted long-term potentiation (LTP), impaired special learning, and altered hippocampal development. | ||
| 005091 | 129S-Pnpla6tm1Blw/J | Repository-Cryopreserved |
| Homozygous null mice have an embryonic lethal phenotype, failing to develop past embryonic day 8.5. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and are more active than wildtype littermates. A reduced level of protein gene product is detected by immunoprecipitation and Western blot analysis of brain, testes and kidney, but protein levels are not reduced in liver. Beta galactosidase activity in heterozygotes aged embryonic day 13.5 is found in the developing lens and spinal cord. In adult heterozygotes, beta galactosidase activity is detected throughout the brain, especially in the cerebellar Purkinje cells and hippocampus. Beta galactosidase activity patterns mimic the endogenous gene expression pattern. NTE activity in brain tissue is reduced by 40%. Heterozygotes are more sensitive to organophosphate toxicity with increased motor activity and mortality. This mutant mouse strain may be useful in studies of neuropathological hyperactivity, G
..... For more information please see the full descriiption on the strain data sheet | ||
| 003117 | 129S-Ssttm1Ute/J | |