Search Criteria: Research Area is "Research Tools: Endocrine Deficiency Research"
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 007005 | 129S-Scg5tm1Led/J | Repository- Live |
| The following text reflects the phenotype reported by the donating investigator on a "129Sv" genetic background (probably "Taconic Sv129" (129S6/SvEvJ)). While heterozygotes are viable and fertile, mice homozygous for this mutation (7B2-null) die in prepubertal or pubertal ages (5 weeks) with severe cardio-respiratory failure, convulsions, and hypothermia. No transcripts are detected in brain tissue from the targeted gene. 7B2 null mice are unable to make an active form of prohormone convertase 2 (PC2) and have high circulating corticosterone. Homozygotes on the 129S genetic background exhibit Cushing's-like disease pathologies of liver, pancreas, and pituitary; including pituitary-dependent hyperadrenocorticosteronism, severe hypoglycemia, hyperproinsulinemia, adrenal hypertrophy, pituitary hypotrophy, and altered islet cell morphology. 7B2-null mice develop the disease from intermediate lobe ACTH hypersecretion (rather than from pituitary adenomas). Other abnormalities include thinni
..... For more information please see the full phenotype on the strain data sheet | ||
| 006411 | B6.129-Gasttm1(INS)Ez/J | Repository- Live |
| Mice heterozygous for this "G-InsKi" allele are viable and fertile. Human insulin expressed from this mutant allele retains full biological activity. Expression of human insulin is specific to gastrin-expressing cells (G cells of the antral stomach and some duodenum cells), and is released into portal circulation in response to the same meal-associated stimuli that control gastrin release. Heterozygous mice exhibit normal blood glucose levels, and toxic hypoglycemia is not observed. The donating investigators report that human insulin levels are sufficient to activate insulin signaling cascades in the liver but not in skeletal muscle. These mutant mice may be useful for diabetes and obesity research, specifically for studying the molecular and physiological mechanisms by which the hepatic action of transgenic insulin prolongs the survival of diabetic mice (e.g. Ins2Akita mutant mice). | ||
| 006879 | B6.129-Scd2tm1Myz/J | Repository- Live |
| While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die within 24 hours of birth. Brain tissues from homozygous mice show no expression from the targeted gene. Homozygotes exhibit neonatal lethality with 100% penetrance on this genetic background (less penetrant on 129SvEv genetic background) likely due to severe skin permeability barrier abnormalities. Null mice also have abnormal epidermal morphology and abnormal lipid homeostasis in the skin and liver. These mutant mice may be useful in studying monounsaturated fatty acid synthesis, lipid biosynthesis and metabolism, cholesterol homeostasis, and skin disease, as well as obesity and diabetes. | ||
| 006333 | B6.FVB(Cg)-Tg(Neurog3-cre)C1Able/J | Repository- Live |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Expression of the transgene is directed by a neurogenin 3 promoter. Tissues where Cre recombinase expression is detected include the small intestine (base of intestinal crypts) and fetal pancreatic epithelial cells. Cre activity has been shown in islets of the adult pancreas, small intestine enteroendocrine cells, endocrine portions of the stomach, all pancreatic endocrine cells, and in some non-endocrine intestinal cells. When bred with a mouse containing a loxP site-flanked sequence of interest, Cre-mediated recombination results in deletion of the flanked gene in the tissues that normally express neurogenin 3.
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. It should be not
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| 005939 | B6;129S6-Insig1tm1Mbjg Insig2tm1Mbjg/J | Repository- Live |
| Mice homozygous for both targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This double mutant has normal expression of Insig1 and no Insig2 gene expression or protein in liver. As the Insig1 mutant locus contains a loxP, frt-flanked exon 1, Cre-mediated deletion of exon 1 (encoding amino acids 1-113) terminates gene function. Double homozygous mutant mice die in utero some time after embryonic day 18.5. These mice may be useful in studies of cholesterol synthesis and feedback suppression, sterol regulatory element-binding protein (SREBP) processing pathways, liver metabolism and storage functions, and may have use in insulin-related topics such as diabetes and endocrine/exocrine function. | ||
| 007678 | B6;SJL-Tg(KRT14-rtTA)208Jek/J | Repository- Live |
| Homozygous females and hemizygous males carrying this X-linked K14-rtTA transgene (K14-rtTetA(X) or rtTAX) are viable and fertile. These mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the human keratin 14 promoter. As the transgene is located on the X chromosome, random inactivation of the X chromosome may result in mosaic rtTA expression patterns in female mice. When mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE or tetO), expression of the target gene in the basal cells of the squamous epithelia and in the outer root sheath of the hair follicles is induced with administration of the tetracycline analog, doxycycline (dox). These K14-rtTA mice provide a Tet-On tool that allows the inducible expression of genes in skin cells. | ||
| 006043 | B6;SJL-Tg(Oxt/EGFP)AI03Wsy/J | Repository- Live |
| Hemizygous mice are viable and fertile with no gross or behavioral abnormalities. This transgene expresses an enhanced green fluorescent protein (EGFP) fused to the end of the neurophysin at the C-terminus of the oxytocin pre-prohormone. The transgene is selectively expressed in oxytocin-magnocellular neurons of the paraventricular and supraoptic nuclei of the hypothalamus. The fusion protein is faithfully trafficked to secretory granules and transported to neurosecretory terminals in the neurohypophysis, where the EGFP fluorescence undergoes depolarization-induced calcium-dependent secretion. Immunohistochemical detection of EGFP in individual oxytocin-magnocellular neurons is suggested as intrinsic fluorescence is low. However, the endogenous fluorescence in the neural lobes is sufficiently intense to image secretory events in individual oxytocin nerve terminals (neurosecretosomes) isolated from the posterior pituitary. These mice may be useful in studies of hormone biology, pharmaco
..... For more information please see the full phenotype on the strain data sheet | ||
| 006699 | C57BL/6J-Pcsk1N222D/J | Repository- Live |
| Mice homozygous for this ENU-induced "Pc1N222D" mutation are viable and fertile, although the donating investigator reports that homozygous breeders have diminished reproductive performance. Unlike mice homozygous for the traditional knockout allele, Pc1N222D homozygotes are not runted. Homozygous mice exhibit obesity, abnormal proinsulin processing and multiple endocrinological defects. Increased energy intake and a more efficient metabolism contribute to the obesity. Defective proinsulin processing leads to glucose intolerance, but neither insulin resistance nor diabetes develop despite obesity. Obesity is associated with impaired autocatalytic and neuropeptide processing. These mutant mice are a model of human PC1 deficiency, and may be useful in studying obesity, fat metabolism, propeptide processing, and neuroendocrinology. | ||
| 005965 | STOCK Tg(Pomc1-cre)16Lowl/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre activity is demonstrable in brain area neurons involved in the control of food intake (arcuate nucleus (hypothalamus) and solitary tract nucleus (hindbrain)). 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 Pomc1. The mice may be useful in studies of obesity, food intake, hunger, endocrine and exocrine function, and for tissue specific gene targeting. | ||
| 005989 | 129;FVB-Tg(PTH-cre)4167Slib/J | Repository-Cryopreserved |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre activity is observed only in parathyroid tissue; no activity is seen in thyroid, muscle, lymph node, trachea, thymus, salivary tissues, lung, heart, liver, brain, stomach, spleen, kidney, large intestine, small intestine, and pancreas. When bred with any mouse containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in parathyroid-specific deletion of the flanked genome. These transgenic mice may be useful in generating mouse models of parathyroid-specific deletion of genes of interest, such as multiple endocrine neoplasia type 1, extracellular calcium-sensing receptor, and vitamin D receptor. | ||
| 005109 | 129S(FVB)-Men1tm1.2Ctre/J | Repository-Cryopreserved |
| These mice possess loxP sites flanking exons 3 to 8 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 bred to a strain expressing Cre recombinase in pancreatic beta cells (see Stock No. 003573 for example), this mutant mouse strain may be useful in studies of pancreatic islet adenomas. | ||
| 003462 | B6.129S1-Thrbtm1Df/J | Repository-Cryopreserved |
| Mice homozygous for the Thrbtm1Df targeted mutation are viable and fertile displaying normal growth rates. Homozygous mutant mice exhibit goiter and elevated levels of both thyroid hormone and thyroid stimulating hormone. Defects in liver responses to thyroid hormone and subtle behavioral abnormalities are observed. The mice fail to develop normal hearing, as assessed by impaired auditory-evoked brainstem responses, and are susceptible to audiogenic seizures. This strain provides a recessive model for the human syndrome of generalized thyroid hormone resistance (GTHR). | ||
| 006086 | B6.SJL-Tg(HBB-GH1)420King/J | Repository-Cryopreserved |
| Mice hemizygous for this transgene are viable. While males are fertile, transgenic females are unreliable breeders and mothers. Homozygotes are sterile. In both fetal and adult tissues, erythroid-specific expression of the transgene is observed. Transgenic mice have 120-150% greater mature body mass and increased bone mass. The donating investigator also reports transgenic mice have increased dermatological stiffness and toughness. Transgenic mice have a characteristic coat with few guard hairs compared to wildtype littermates. These mice may be useful in studies of bone formation and development, dermatology, and acromegaly. | ||
| 002437 | FVB/N-Tg(MMTV-Notch4)3Rnc/J | Repository-Cryopreserved |
| Male mice transgenic for the Notch4 gene (previously called Int3) are sterile, and females fail to lactate. Mammary tissue of females does not develop completely, exhibiting dramatic inhibition of alveolar-lobular development and reduced penetration of the mammary fat pad by ductal epithelium. Glandular epithelia of tissues expressing the activated form of Notch4 generally display severe ductal hyperplasia. Salivary glands fail to differentiate completely. Male transgenic mice exhibit severe epididymal hyperplasia, which is thought to be the cause of their sterility. Both male and female mice develop focal adenomas of the mammary and salivary glands. | ||
| 004066 | FVB;129S-Men1tm1.1Ctre/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Men1 gene die in utero at embryonic days 10.5-11.5, exhibiting delayed development often (20%) with defects in cranial/facial formation. At birth, heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. At nine months, ~80% of the heterozygous-null mice develop abnormalities in pancreatic islet cells, the severity of which ranges from hyperplasia to insulin-producing tumors. Parathyroid adenomas are also observed at this age. Tumor incidence is progressive, with occurrences in multiple endocrine tissues (pancreatic islets, parathyroids, thyroid, adrenal cortex, pituitary) by sixteen months of age. | ||
| 005701 | STOCK Pdx1tm1Macd/J | Repository-Cryopreserved |
| Mice homozygous for the targeted mutation fail to develop a pancreas. Heterozygous mice have normal pancreas development but partially impaired glucose tolerance in adulthood. The substitution of the targeted gene with tTAoff inactivates the endogenous allele and places tTAoff expression under the control of the endogenous transcriptional regulatory sequences. tTA expression from the modified locus is identical to that of the normal allele; tTA mRNA is detectable in the pancreas but not in other visceral organs or salivary glands. This mutant may be useful in studies of pancreatic endocrine/exocrine function and diabetes. Heterozygotes also can be bred with transgenic mice that express a target gene under the regulation of a tetracycline-responsive element (TRE; tetO) for pancreas-specific applications.
This mutant was originally designed to be mated with mutant mice with a TRE-controlled transgene coding for the endogenous Pdx1 (Ipf1) gene alon
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| 005667 | STOCK Tg(Neurog3-cre)C1Able/J | Repository-Cryopreserved |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Expression of the transgene is directed by a neurogenin 3 promoter. Tissues where Cre recombinase expression is detected include the small intestine (base of intestinal crypts) and fetal pancreatic epithelial cells. Cre activity has been shown in islets of the adult pancreas, small intestine enteroendocrine cells, endocrine portions of the stomach, all pancreatic endocrine cells, and in some non-endocrine intestinal cells. When bred with a mouse containing a loxP site-flanked sequence of interest, Cre-mediated recombination results in deletion of the flanked gene in the tissues that normally express neurogenin 3. | ||
| 005699 | STOCK Tg(tetO-Ipf1,EGFP)956.6Macd/J | Repository-Cryopreserved |
| Mice hemizygous for the transgene are viable, fertile, normal in size, and do not display any behavioral abnormalities. At the Jackson Laboratory, no homozygous mice were produced from mating hemizygotes together, suggesting that homozygous transgenic animals die in utero. Expression of the bicistronic transgene is under the regulation of a tetracycline promoter element (TRE; tetO). By themselves, these transgenic mice do not express EGFP, but when these mice are mated with a second transgenic strain expressing tetracycline-transactivator (tTA) protein under the control of a tissue-specific promoter, Ipf1 and EGFP are highly expressed in the appropriate tissue of bitransgenic offspring.
This mouse was originally designed to be mated to an apancreatic targeted mutant with tTAoff in place of the endogenous Ipf1 gene (see Stock No. 005701). The combined mutations allow normal pancreatic dev
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