Search Criteria: Research Area is "Developmental Biology Research: Internal/Organ Defects (brain)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 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. | ||
| 008217 | B6.129S1-Car4tm1Sly/J | Repository- Live |
| Mice that are homozygous for this targeted mutation exhibit decreased sensitivity to an inhibitor of pH regulation (benzolamide) in the extracellular space in the hippocampus when compared to wildtype controls. No gene product (mRNA or protein) is detected by RT-PCR or Western blot analysis of brain, heart, kidney, liver, and muscle tissue. Exons 1b, 2, and 3, a portion of exon 4, which encode three active-site His residues, are disrupted and results in early termination in exon 4. Fewer than expected homozygotes are produced from heterozygote crosses (with even fewer female homozygotes produced). Surviving homozygotes from heterozygote crosses are fertile when crossed to wildtype mice, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous crosses produce small litters and pups do not survive. This mutant mouse strain may be useful in neuronal physiology related studies, especially those involving pH shifts that accompany neuronal activity.
..... For more information please see the full descriiption on the strain data sheet | ||
| 005359 | B6.Cg-Tg(Camk2a-cre)T29-1Stl/J | Repository- Live |
| Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the Cre recombinase under the control of the mouse calcium/calmodulin-dependent protein kinase II alpha promoter. Cre recombinase expression is detected in the forebrain, specifically to the CA1 pyramidal cell layer in the hippocampus. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination occurs in the pyramidal cell layer. | ||
| 005992 | STOCK Efna2tm1Jgf Efna5tm1Ddmo/J | Repository- Live |
| Mice homozygous for both targeted mutations are viable, fertile, and normal in size. 10-20% of females homozygous at both loci neglect their litters. Double homozygous mice have no endogenous protein expression in inferior colliculus (IC) or superior colliculus (SC), and thus lack the concentration gradient created by the endogenous proteins across the midbrain in wildtype mice. Temporal and nasal retinal axon termination is severely altered: multiple ectopic aborizations in the SC indicate abnormalities in both anteroposterior and dorsoventral topography. Following surgical ablation of portions of the midbrain (including IC and SC), cross-modal innervation by retinal neurons is greater in double homozygous mutants compared to wildtype. Mice heterozygous at both loci have greater reproductive performance compared to homozygotes. Further, double heterozygotes have temporal (but not nasal) retinal axon aborization in the SC with diminished frequency and severity. These ephrin A2/ephrin A
..... For more information please see the full descriiption on the strain data sheet | ||
| 006207 | STOCK Tg(Pcp2-cre)1Amc/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 parasagittal domains of the cerebellum beginning at embryonic day 17 (E17). At E19, low level expression is observed in the most rostral lobe of cerebellum and expression broadens until all Purkinje cells express the transgene in adult mice. When bred with any mouse containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the flanked genome. These transgenic mice may be useful in studies utilizing “Cre-lox” technology, specifically regarding the nervous system, development and patterning of cerebellum, and cerebellar hypotrophy converse of Lhermitte-Duclos. | ||
| 002434 | B6 x BALB/cByJ-Kcna1mceph/J | Repository-Cryopreserved |
| Mice homozygous for the megencephaly spontaneous mutation (mceph) are characterized by a 25% increase in brain size in the first 8 months of life. This defect can be distinguished from macrocephaly, an enlarged head, which usually occurs as a consequence of congenital hydrocephalus. By 3-4 weeks of age, mice homozygous for the mceph mutation have a subtle shakiness in their gate and by 4-6 weeks are found to sit on their haunches using their tails as support with their forelimbs held loosely in front of them. They maintain this posture for a period ranging from 30 seconds to several minutes before returning to normal. They have lower overall body weights than their wildtype littermates and are hypersensitive to sharp sounds. Electroencephalogram readings for homozygotes are normal. Neither male nor female mutants breed, but ovarian transplant from homozygous donors is successful for colony maintenance. Homozygotes have an increased brain mass that is evident by one t
..... For more information please see the full descriiption on the strain data sheet | ||
| 007666 | B6.129S6-Jmjd6tm1Flv/J | Repository-Cryopreserved |
| Homozygotes are defective in removing apoptotic cells, which accumulate in the lung and brain, causing abnormal development and neonatal lethality. Approximately 15% of the homozygotes manifest a hyperplastic brain phenotype resembling that of mice deficient in other cell death-associated genes. The absence of expression in homozygous mice has been confirmed by Northern blot analysis of embryonic fibroblasts. This strain may be useful in studies of mammalian organogenesis, respiratory distress syndromes and congenital brain malformations. | ||
| 006566 | B6.129S6-Ppt1tm1Hof/SopJ | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by immunoassay. Palmitoyl-protein thioesterase activity in the brain of the mutant is reduced to background levels. Although healthy at birth, by age four to five months, mutant mice display lack of grooming and an abnormal gait that progresses to hind limb paralysis. By six to eight months of age mutant mice have a low body weight and display an abnormal clasping behavior. Aggressive behavior results in fighting and dermatitis due to bite wounds. By seven months of age, mortality is 50% with very few mice surviving beyond ten months of age. Myoclonic jerks and seizures manifest at age three to four months. Strong rapid hind limb seizures ("popcorn" seizures) that propel mice several feet also occur. Brain size of the mutant mice is reduced. Histologically, mutant brains show neuronal loss and apoptosis in
..... For more information please see the full descriiption on the strain data sheet | ||
| 004341 | B6.129X-Cxcr4tm1Qma/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Cxcr4 gene die perinatally, with ~30% dying by embryonic day 18.5. Viable embryos are slightly smaller than wild type mice and exhibit vascular congestion in the kidneys, interstitial hemorrhages, and abnormalities in bone marrow and cerebellum. Homozygote embryos also show reduced B-lymphopoiesis, reduced myelopoiesis in fetal liver and an absence of myelopoiesis in bone marrow. Histological examination reveals a distorted architecture in the tissues if the cerebellum, featuring an attenuated external granule cell layer and an ectopic placement of Purkinje cells. Cxcr4 encodes a receptor commonly called CXCR4, the ligand of which is the chemokine stromal cell-derived factor 1 (SDF-1), an important regulator of hematopoietic cell development, migration and proliferation. CXCR4 also functions as a coreceptor for the entry of T-tropic strains of HIV-1 into CD4+ T cells. In an attempt to offer alleles on well-charac
..... | ||
| 005642 | B6.Cg-Clutm1Jakh/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size, and do not display any behavioral abnormalities. No protein is detected in serum, liver, or brain and in situ hybridization shows no mRNA in heart. This mutant has been studied for different functions on different backgrounds. On the Swiss Black outbred background, aging homozygous mutant mice develop a progressive glomerulopathy characterized by deposition of tubulo-fibrillary immune complexes devoid of inflammation or necrosis. On the FVB/N background, homozygous null mice with chemically induced autoimmune myocarditis show severe and diffuse lesions with postinflammatory functional impairment. Induced skin carcinogenesis is more severe than wildtype. On the C57BL/6 background, homozygotes given a hypoxia-ischemia brain injury (modeling cerebral palsy) had 50% less brain injury compared to wild type. Conversely, mutants have less neuroprotective properties after permanent focal cerebral isc
..... For more information please see the full descriiption on the strain data sheet | ||
| 000518 | B6.Cg-Usp14ax-J/J | Repository-Cryopreserved |
| The first outward sign of homozygosity for the recessive mutation Usp14ax-J is an unsteady gait, particularly in the hind quarters, that can be detected by approximately 2 weeks of age. These pups often show difficulty in righting themselves when turned on their backs. They have a rapid tremor that is most apparent when they are active. Extensor paralysis progresses and wasting of the hind quarters ensues until the hind quarters are not functional and the mouse can not sit upright or move except through the use of onlyits front limbs. Although death is premature, viability in the first two to three weeks is not diminished. At 18 days of age these mutants weigh an average of 15% less than wildtype controls and by 45 days this difference is increased such that they weigh 50-60% less than wildtype controls. Homozygotes do not breed. The lumbar vertebrae are slightly shorter than normal with shorter spinous processes and more elongate foramen. These homozygotes have defec
..... For more information please see the full descriiption on the strain data sheet | ||
| 001271 | B6.RBF-Nek1kat/J | Repository-Cryopreserved |
| The phenotype associated with the Nek1kat-2J allele is more severe than that of the Nek1kat allele. Mice homozygous for Nek1kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1Kat-2J
..... For more information please see the full descriiption on the strain data sheet | ||
| 004313 | B6;129-Ppt1tm1Hof/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by immunoassay. Palmitoyl-protein thioesterase activity in the brain of the mutant is reduced to background levels. Although healthy at birth, by age four to five months, mutant mice display lack of grooming and an abnormal gait that progresses to hind limb paralysis. By six to eight months of age mutant mice have a low body weight and display an abnormal clasping behavior. Aggressive behavior results in fighting and dermatitis due to bite wounds. By seven months of age, mortality is 50% with very few mice surviving beyond ten months of age. Myoclonic jerks and seizures manifest at age three to four months. Strong rapid hind limb seizures ("popcorn" seizures) that propel mice several feet also occur. Brain size of the mutant mice is reduced. Histologically, mutant brains show neuronal loss and apoptosis in
..... For more information please see the full descriiption on the strain data sheet | ||
| 003120 | B6;129S7-L1camtm1Sor/J | Repository-Cryopreserved |
| The L1 gene is localized to the X chromosome. As a result, hemizygous males are affected and the mutation has to be propagated through females. Male mice hemizygous for the L1camtm1Sor targeted mutation have defects in the guidance of axons of the corticospinal tract. A substantial proportion of axons do not take their normal crossed course to the dorsal column at the pyramidal decussation. There is also a varying, but reduced number of corticospinal axons in the dorsal columns of the spinal cord. | ||
| 001035 | B6C3Fe a/a-Napahyh/J | Repository-Cryopreserved |
| Although no overt phenotype is appearant in newborn hyh mice, they have dilated lateral ventricles. By 2 weeks of age, an outward phenotype of a domed head and a hop gait is apparent. Dissection and histological examination reveal "hydrocephalus of lateral and third ventricles and of the caudal aspects of the cerebreal aquiduct" increasing in severity with age (Bronson et al., 1990). Homozygotes have a decreased lifespan usually dying before 2 months of age. Some homozygotes will live for several months, but usually will not breed. | ||
| 004317 | BALB/cBy-Gulosfx/J | Repository-Cryopreserved |
| The sfx phenotype is not apparent until shortly after weaning age. By 26-30 days of age, homozygotes display decreased mobility, diminished weight gain, and more scruffy appearance than their heterozygous or wildtype siblings. Dissection reveals smaller spleen and thymus and increased kidney and brain weights. A reduction in bone mass is accompanied by a paucity of mature osteoblasts on bone surfaces, a subtle reduction of chrondrocytes in epiphyseal-plate columns, growth plate arrest in long bones, and other architectural abnormalities. Bone analysis shows sponteneous fractures both in large bones and smaller ones such as metacarpals. Serum analysis shows a decrease in calcium, inorganic phosphate, alkaline phosphatase, osteocalcin, and insulin-like growth factor 1. These homozygotes also have a reduction in the number of both the red and white blood cells. Homozygotes are fragile and must be handled with great care. (Beamer et al., 2000.) | ||
| 005706 | C57BL/6-Tg(tetO-CDK5R1/GFP)337Lht/J | Repository-Cryopreserved |
| Hemizygous transgenic mice are viable, fertile, normal in size and do not display any behavioral abnormalities. Mice homozygous for this transgene may not be viable. When these transgenic mice are bred with mice expressing the tetracycline-controlled transactivator protein (tTA) under the regulation of a tissue-specific promoter, expression of the CDK5R1/GFP fusion protein in the appropriate tissue of the bitransgenic offspring can be regulated by doxycycline administration. These mice may be useful in studies of Alzheimer's disease and other neurodegenerative tauopathies, amyotrophic lateral sclerosis (ALS), Niemann Pick Type C (NPC) disease, and Parkinson's disease.
Note: this transgenic strain was designed to breed with Tg(Camk2a-tTA) transgenic mice, (Stock No. 003010), a transgenic strain that expresses tTA in forebrain neurons. The resulting bitransgenic offspring exhibit the hallmark phenotype of Alzheimer's disease;
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| 002854 | C57BL/6J-Nek1kat-2J/J | Repository-Cryopreserved |
| The phenotype associated with the Nek1kat-2J allele is more severe than that of the Nek1kat allele. Mice homozygous for Nek1kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1Kat-2J
..... For more information please see the full descriiption on the strain data sheet | ||
| 005744 | C57BL/6J-Relnrl-6J/J | Repository-Cryopreserved |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Relnrl-6J entry. | ||
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