Search Criteria: Research Area is "Endocrine Deficiency Research: Mammary Gland Defects"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 006943 | B6.129S7-B4galt1tm2Shur/J | Repository- Live |
| These mice carry a mutant allele that has a point mutation in the first translation initiation codon in exon 1, which initiates translation of the long isoform of beta 1,4-galactosyltransferase. The second translation initiation codon in exon 1 is not affected. These mice express only the shorter isoform of beta 1,4-galactosyltransferase. No long isoform protein is detected in mammary tissue by Western blot analysis. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Total Beta 1,4-galactosyltransferase activity is reduced to 72% of wildtype levels in mammary gland epithelial cells while activity on mammary epithelial cell surfaces is diminished by over 60%. Sperm and testis exhibit near wildtype levels of enzyme activity and glycoprotein galactosylation. The short isoform is expressed ectopically in sperm. Although able to undergo normal acrosomal exocytosis induced by calcium ionoph
..... For more information please see the full descriiption on the strain data sheet | ||
| 008041 | B6;129-Sirt1tm1Ygu/J | Repository- Live |
| Mice homozygous for this targeted allele (SirT1co/co) are viable and fertile. A loxP-flanked neomycin cassette just upstream of exon 4 and a third loxP site downstream of exon 4 were inserted to create this targeted mutant Sirt1 allele. The floxed mutation does not affect SIRT1 protein expression in MEFs or mammary gland tissue in homozygotes. When bred to mice that express Cre recombinase, the resulting offspring have exon 4 (encoding an evolutionarily conserved Sir2 motif) deleted in cre-expressing tissue(s); (the donating investigator reports only one recombination event: complete removal of the neomycin cassette and exon 4, leaving a single loxp). These SirT1co/co mice may be useful in generating conditional mutants for studying transcriptional regulation and the role of estrogen, insulin growth factor-1 (IGF-1), and transcription factors (including NF-kappaB) in mammary gland development, mammary cancer, apoptosis, and metabolic di
..... For more information please see the full descriiption on the strain data sheet | ||
| 007810 | C.129-Stat5btm1Hwd/J | Repository- Live |
| Mice that are heterozygous 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 and immunoblot analysis of liver, spleen, mammary gland, thymus, kidney or skeletal muscle from homozygous animals. Levels of the closely related Stat5a gene products (mRNA and protein) are unaffected in thymus and spleen. At 4 - 5 weeks of age, male homozygotes are smaller in size and have a reduced body weight (27% lighter than wildtype controls) when compared to wildtype. Female homozygotes exhibit spontaneous abortion between day 8 and 17 of pregnancy and have impaired lactation. Pups (independent of genotype) born to heterozygous females have higher perinatal death than pups born to wildtype females. Some homozygotes have pale and enlarged livers. Homozygotes have less adipose tissue than wildtype controls, exhibit abnormal gene expression in liver, reduced insuli
..... For more information please see the full descriiption on the strain data sheet | ||
| 006873 | STOCK Cebpbtm1Vpo/J | Repository- Live |
| Significant numbers of mice homozygous for this C/EBP-beta mutationon this mixed genetic background die perinatally due to hypoglycemia and a failure to mobilize glycogen. Homozygous males that survive to adulthood are fertile, but females are sterile, and display altered mammary duct formation. Macrophages isolated from homozygous mutant mice have impaired bactericidal activity. Surviving homozygotes exhibit fasting hypoglycemia, with reduced plasma insulin, plasma lipids, and free fatty acids (FFAs), and impaired hepatic glucose production. Further, they have a blunted response to glucagon and adrenaline primarily due to altered levels of hepatic cAMP production and reduced protein kinase A activity. Homozygous mice are resistant to obesity and have increased carbon dioxide production from increased metabolism in the brown adipose tissue and muscle. On a high-fat diet, homozygotes are protected from obesity and fatty liver due to reduced hepatic expression of lipogenic genes. Homozyg
..... For more information please see the full descriiption on the strain data sheet | ||
| 003142 | B6.129P2-Prlrtm1Cnp/J | Repository-Cryopreserved |
| There is complete female sterility due to abberant estrous cycles, abnormal preimplantation development of eggs, no implantation of blastocysts, lack of pseudopregnancy. Males show slightly delayed fertility. Mammary development is markedly affected. Homozygotes have no mammary development and do not lactate. Heterozygotes are unable to lactate after the first pregnancies, but attain some degree of lactation as they age or after multiple pregnancies. Serum prolactin levels are increased 60 - 100 fold in both males and females. Maternal behavior is diminished in pimiparous and nulliparous animals. Bone remodelling is decreased in homozygote mutants. | ||
| 003808 | B6.129S2(Cg)-Prltm1Hmn/J | Repository-Cryopreserved |
| Mice that are homozygous for the null Prl allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null females have an irregular estrous cycle and are completely infertile. Homozygous null males and heterozygous females exhibit no fertility problems. The targeted insertion of a neomycin resistance gene into exon 4 results in a truncated Prl transcript that produces an 11 kDa prolactin protein that lacks any detectable bioactivity. Mammary gland development is marked by an absence of terminal or lateral lobulation. The disruption of the prolactin gene appears to have no effects on the hematopoietic system. | ||
| 002713 | B6;129S-Oxttm1Wsy/J | Repository-Cryopreserved |
| Mice homozygous for the Oxttm1Wsy targeted mutation are viable and fertile. Females are able to successfully mate, deliver and produce milk however milk injection is impaired. Pups do not successfully suckle and must be fostered to survive. Oxytocin injection restores milk injection in response to suckling. Homozygotes displayed reduced aggressive behavior relative to heterozygotes and wild-type mice. | ||
| 002499 | C57BL/6J-Tg(WapIGFBP3)67Dlr/J | Repository-Cryopreserved |
| Mice homozygous for the WapIGFBP3 transgene are viable and fertile. The transgene is expressed at high levels during lactation and post-lactation. There were no obvious changes in mammary gland histomorphology during lactation, but at 5 to 10 days post-laction, there was a delay in involution and decreased apoptosis. This phenotype is identical to that of the C57BL/6J-TgN(WapIgf1)39Dlr strain mice. | ||
| 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. | ||
| 003258 | STOCK Igf1tm1Ts/ImJ | Repository-Cryopreserved |
| The majority of mice homozygous for the Igf1tm1Tstargeted mutation die perinatally. Only ~4% of homozygotes survive beyond birth for up to 4 months of age. Heterozygotes have serum levels of IGF-1 that are 37% lower than in wild type mice. Body size is, proportionally, 10-20% smaller than that of normal wild type siblings, with no apparent histological abnormalities. | ||
| 003259 | STOCK Igf1tm2Ts/ImJ | Repository-Cryopreserved |
| Mice homozygous for the Igf1tm2Ts mutation (also referred to as the Igf1m/m midi targeted insertion) are viable and fertile, but are small in size, reaching only approximately 60 - 65% the weight of their wild type siblings. Serum levels of IGF-1 in these mutants is 30% of wild type values. They have no gross histological abnormalities. Arterial blood pressure is higher in Igf1m/m mice than in wild type controls | ||
| 000579 | STOCK a tp/J | Repository-Cryopreserved |
| Taupe is a recessive spontaneous mutation that causes a lightening of the coat color such that a/a tp/tp mice are slate grey. The coat color is similar to that of the ruby (Hps5ru) mutation but the eye color is not affected and the belly fur is lighter in color with yellow at the margins. The homozygous females do not have normal nipple development, although the mammary ducts and alveoli develop normally. These females also have difficulty with pregnancy and birth. They can not rear their pups even if the pups are born alive so this strain is maintained by breeding heterozygous females to homozygous males. (Fielder, 1952; Fielder, 1950.) | ||
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