Search Criteria: Research Area is "Endocrine Deficiency Research: Gastrointestinal Defects"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 006365 | 129-Cckartm1Kpn Cckbrtm1Kpn/J | Repository- Live |
| Mice that are homozygous for both of the targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The donating investigator reports that the double mutants have a combined phenotype.
No CCKBR receptor function was detected in competition binding assay of brain (cerebral plasma) membranes. When compared to wildtype, gastric pH in homozygotes is higher, pH 5.2, after overnight fast. Histological analysis reveals diminished parietal cell, enterochromaffin-like cell and antral comatostatin-producing D cell densities. An increase in the number of gastrin-producing G cells is observed. There is an increased number of H+, K+ -ATPase immunoreactive negative cells and abnormal distribution of parietal cells in oxyntic glands. Circulating gastrin levels are 10-fold higher in homozygotes. No CCKAR receptor function was detected in competition binding assay of pancreatic membranes. Homozygotes do not exhibit decreased ..... For more information please see the full descriiption on the strain data sheet | ||
| 006367 | 129-Cckartm1Kpn/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 receptor function was detected in competition binding assay of pancreatic membranes. Mice homozygous for the targeted mutation do not exhibit decreased food intake due to peritoneal injection of cholecystokinin. Baseline food and water intake and body weight is normal in mutant mice. These mutant mice have larger gallbladder volumes and are more likely to develop spontaneous gallstones than wildtype controls. Gastric function is impaired due to diminished intestinal lipid feedback response. Small-intestine transit time is increased in mutant mice. When fed a lithogenic diet, mutant mice have an increase in biliary cholesterol secretion rates, when compared to the wildtype. Although the total number of olfactory-gonadotropin-releasing hormone-1 neuroendocrine (GnRH-1)neurons is the same in embryonic day 14.5 aged mutant and wildtype
..... For more information please see the full descriiption on the strain data sheet | ||
| 006369 | 129-Cckbrtm1Kpn/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 receptor function was detected in competition binding assay of brain (cerebral plasma) membranes. When compared to wildtype, gastric pH in homozygotes is higher, pH 5.2, after overnight fast. Histological analysis reveals diminished parietal cell, enterochromaffin-like cell (ECL) and antral comatostatin-producing D cell densities. An increase in the number of gastrin-producing G cells is observed. There is an increased number of H+, K+ -ATPase immunoreactive negative cells and abnormal distribution of parietal cells in oxyntic glands. Circulating gastrin levels are 10-fold higher in homozygotes. Gastric mucosal histamine levels are greatly reduced and histamine-immunoreactive ECL cells are absent. This mutant mouse strain may be useful in studies of hypochlorhydria, hypergastinemia, gastric antral endocrine regulation, and
..... For more information please see the full descriiption on the strain data sheet | ||
| 008243 | 129-Tff3tm1Dkpy/J | Repository- Live |
| Mice homozygous for this intestinal trefoil factor (ITF or Tff3) mutant allele are viable and fertile with no RNA or protein expression of the targeted gene in the gastrointestinal tract. Homozygous mice exhibit impaired physiological migration of intestinal epithelium to the mucosal surface, have impaired mucosal healing and increased susceptibility to dextran sulfate sodium (DSS)- induced colitis, and are more susceptible to chemotherapy and radiation-induced mucositis. These intestinal trefoil factor (ITF or Tff3) mutant mice may be useful in studying gastrointestinal tract injury (including inflammatory bowel diseases), maintenance of the mucosal barrier, migration and turnover of the intestinal epithelium, and therapies for colon cancer. | ||
| 008117 | B6.129S4(129S6)-Ssttm1Ute/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. Homozygotes exhibit increased baseline plasma growth hormone, corticosterone and total ghrelin levels compared to wildtype. Mutant mice have impaired motor performance ability. Somatostatin-deficient mice have enlarged stomachs with an increased number of parietal cells and hyperchlorhydria. Hippocampal neprilysin activity is diminished. Compared to wildtype controls, amyloid beta 42 peptides levels are elevated in the hippocampus. This mutant mouse strain may be useful in studies of gastric homeostasis, learning and memory and endocrinology. | ||
| 006133 | B6.129S4-Vdrtm1Mbd/J | Repository- Live |
| Heterozygous mice are phenotypically indistinguishable from wildtype siblings. Homozygous mice are viable and fertile with normal survival until approximately 14 months. RNA isolated from the intestine and kidney show a truncated deletion of the second zinc finger coding region followed by a premature termination codon, resulting in the absence of receptor protein. Homozygous mice exhibit an identical phenotype as the human disease hereditary vitamin D-dependent rickets type II (HVDDR). As early as 21 days of age, mutant mice demonstrate hypocalcemia, hypophosphatemia, hyperparathyroidism, increased serum parathyroid hormone, abnormal blood mineral levels, and growth retardation. In addition, renin and plasma angiotensin II levels are increased. Homozygous mice are hypertensive and exhibit cardiachypertrophy. At 4 weeks of age, homozygous mice exhibit perioral and periorbital alopecia that progresses over the entire body by 4 months of age. Rickets and osteomalacia develop by 35 days.
..... For more information please see the full descriiption on the strain data sheet | ||
| 000528 | B6.Cg-PhexHyp/J | Repository- Live |
| Hypophosphatemia (PhexHyp) is an X-linked semidominant mutation that causes defects in phospate metabolism. It is allelic with the gyro mutation (PhexGy) but hypophosphatemia mutant mice do not circle. Hemizygous males and heterozygous females can be recognized at 20 to 30 days of age by their shortened hindlimbs and tail. They have reduced body size which persists throughout life, and skeletal changes resembling rickets. Hemizygous males are more affected than heterozygous females. Viability is normal in both sexes, but heterozygous females show better fertility than hemizygous males. | ||
| 006956 | NOD.Cg-Vdrtm1Ska/CmatJ | Repository- Live |
| Heterozygous mice are viable, fertile, and phenotypically indistinguishable from wildtype siblings. Homozygous mutant mice are viable but infertile. No VDR mRNA is detected by RT-PCR in samples from the intestine or kidney or from homozygous mutant embryo. Increased expression of CTP27B1 and reduced expression of CYP24A1 and calbindin-D9k is detected by RT-PCR in samples from VDR-deficient kidneys. Although mice homozygous for this targeted mutation are viable, shortly after weaning they exhibit dysmorphic features including a flat face and short nose, alopecia, growth retardation, and skeletal defects including hypocalcaemia, decreased bone mineral density, widened growth plates with hypomineralization, less trabeculae and thicker osteo seams. Homozygous mutant mice exhibit metabolic imbalances including abnormally high and low levels of 1,25(OH),2D3 and 25(OH)D3, respectively and abnormal cytokine and chemokine profiles.
Homozygous mice exhibit normal pancreatic islet archite
..... | ||
| 003126 | B6.129X1-Grprtm1Jfb/J | Repository-Cryopreserved |
| Mice homozygous (females) or hemizygous (males) for the X-linked Grprtm1Jfb targeted mutation are viable with no gross phenotypic abnormalities observed. There is a deficiency in bombesin-induced mediation of satiety as measured by glucose intake. A modest increase in body weight is observed in older animals. At 18-20 months of age, hemizygous males (N = 8) are 44.5g ± 5.1 (mean ± std dev) and wildtype littermates (N = 8) are 38.3g ± 5.1 (L. Hampton, unpublished observation). We have recently observed head tilts and bobbing in the hemizygous males in our production colony. The donating investigator of this strain has also observed this phenotype and considers it a mutation not related to the gene. We are working to remove this phenotype, but we will continue to ship from the colony while we finish this process. | ||
| 001723 | CByJ.A-Ttc7fsn/J | Repository-Cryopreserved |
| Homozygous fsn mice suffer from hypochromic and normocytic anemia at birth which becomes more severe with age. The anemia makes the homozygous mice distinguishable as pups because of the pale color of ears and eyes. At 2 weeks of age focal epidermal hyperplasia and inflammation is evident with psoriasiform skin lesions becoming confluent and diffuse in 3-4 week old weanlings. The skin lesions progress to generalized alopecia and shedding of thick white scales. The gross lesions are accompanied by thickening and keratinization of the skin. A progressive paplosquamous disease ensues which is a model for some forms of psoriasis. fsn/fsn mice show hematocrit levels and red blood cell counts that are significantly decreased from birth through adulthood. Consequently the heart, liver and spleen become enlarged but the thymus weight is less than half normal. As the spleen enlarges, the mice also develop a potbellied appearance aiding in homozygous fsn identification. G
..... For more information please see the full descriiption on the strain data sheet | ||
| 001788 | STOCK Tg(Fabp1-GH1)10Bir/J | Repository-Cryopreserved |
| 001400 | STOCK Tg(Fabp1-GH1)5Bir/J | Repository-Cryopreserved |
| 001515 | STOCK Tg(Fabp1-GH1)7Bir/J | Repository-Cryopreserved |
| 001878 | STOCK Tg(IFABP-GH)11Bir/J | Repository-Cryopreserved |
| 001879 | STOCK Tg(IFABP-GH)12Bir/J | Repository-Cryopreserved |
| 001909 | STOCK Tg(IFABP-GH)15Bir/J | Repository-Cryopreserved |
| Obligate hemizygous F1 offspring from founder 54 carried approximately 60 copies of the transgene in tandem head-to-tail arrangement in a single insertion site. Expression of the reporter gene, human growth hormone, is appropriately restricted to the intestine where the duodenum and proximal jejunum show expression levels normal for intestinal fatty acid binding protein, but the distal small intestine shows reduced expression. Resultant serum human growth hormone levels were 6-38 ng/ml which is approximately 1000 times lower than in mice carrying a transgene with an extended I-FABP promoter which includes nucleotides -1178 to +28. Use of the extended (-1178 to +28) promoter also results in a more normal expression in the distal small intestine. (Sweetser et al., 1988.) | ||
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