JAX Mice Database - Apoptosis Research

New strains under development - Research area: Apoptosis Research

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Apoptosis Research

Allele Symbol Strain Description	Stock Number	Strain Name (link to Data Sheet)
Eif2ak4^tm1.1Dron	008452 Under Development for Production	B6;129-Eif2ak4^tm1.1Dron/J
Mice homozygous for the GCN2.KO4^conditional allele (also called GCN2.KO4c) have loxP sites flanking exon XII of the eukaryotic translation initiation factor 2 alpha kinase 4 (Eif2ak4 or GCN2) targeted gene, and may be useful in generating conditional mutations for studying eIF2 (eukaryotic initiation factor 2) phosphorylation in response to environmental stresses (amino acid starvation, proteasome inhibition and UV irradiation).
Eif2ak4^tm1.2Dron	008240 Under Development for Production	B6.129S6-Eif2ak4^tm1.2Dron/J
Mice homozygous for the GCN2.KO4 mutant locus (also called GCN2.KO4^-, GCN2^-, GCN2.KO4^ex, or GCN2-KO) have a deletion of exon XII of the eukaryotic translation initiation factor 2 alpha kinase 4 (Eif2ak4 or GCN2) gene, and may be useful in studying eIF2 (eukaryotic initiation factor 2) phosphorylation in response to environmental stresses (amino acid starvation, proteasome inhibition and UV irradiation).
Gt(ROSA)26Sor^{tm3(CAG-MIRN17-92,-EGFP)Rsky}	008517 Under Development for Production	C57BL/6-Gt(ROSA)26Sor^{tm3(CAG-MIRN17-92,-EGFP)Rsky}/J
These mice harbor the "miR-17-92 transgene" targeted to the Gt(ROSA)26Sor locus. The "miR-17-92 transgene" has a loxP-flanked Neo-STOP cassette preventing transcription of the downstream human miR-17-92 cluster (encoding the precursor of seven miRNA molecules; miR-17-5p, miR-17-3p, miR-18a, miR-19a, miR-20a, miR-19b and miR-92). When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissue(s) resulting in expression of the human miR-17-92 cluster. These miR-17-92 transgenic mice allow inducible expression of the human miR-17-92 cluster which has been associated with lymphomas and other cancers, autoimmune defects, and altered expression of tumor suppressor and pro-apoptotic genes.
Tnf^tm1Gkl	007082 Under Development for Production	CByJ.129S(B6)-Tnf^tm1Gkl/J
Mice homozygous for the Tnf^tm1Gkl targeted mutation may be useful in studies of susceptibility to parasitic amd bacterial infection, endotoxin sensitivity and immune response.
Traf1^tm1Tsi	008074 Under Development for Production	C.129S4-Traf1^tm1Tsi/J
These TRAF1 mutant mice may be useful in studying negative regulation of tumor necrosis factor (TNF) signaling, NF-kB and AP-1 signaling, T cell receptor (TCR)-induced proliferation of T cells, Th2 responses, TRAF1/Bim function in CD8 memory T cell survival, allergic airway diseases and Rheumatoid arthritis, as well as the role of TRAF1 activation in the pathogenesis of lymphomas. Of note, TRAF1 mutant mice are available on either a BALB/c congenic (Stock No. 008074) or C57BL/6 congenic (Stock No. 008076) background.
Trp53^tm1Brn	008462 Under Development for Production	B6.129P2-Trp53^tm1Brn/J
Exons 2-10 of the Trp53 (transformation related protein 53) gene are flanked by loxP sites in this conditional targeted mutation. Mice homozygous for the floxed allele do not show any increase in disease incidence for at least a year. When bred to mice with a cre recombinase gene under the control of a promoter of interest, expression is deleted in the tissue of interest.
Tg(CAG-SAC/EGFP)35Rang	008080 Under Development for Production	B6;C3-Tg(CAG-SAC/EGFP)35Rang/J
These SAC-GFP transgenic mice may be useful as a cancer-resistant model; evading oncogene-mediated tumorigenesis by expressing an archetypical anticancer therapeutic agent (SAC) that is well tolerated in vivo, does not compromise the normal tissue function or life span of the host, and is potent enough at physiologically innocuous levels to concomitantly suppress the NF-kappaB pro-cell survival pathway and induce tumor suppression via apoptosis.
Tg(Ela1-TAg*)289Mjt	008247 Under Development for Production	B6.Cg-Tg(Ela1-TAg*)289Mjt/J
These T1-147 transgenic mice (harboring the E1-T147 transgene) develop metastatic pancreatic acinar cell cancer as a result of expression of the 1-147 amino acid fragment of simian virus 40 large T antigen (TAg) directed to pancreatic acinar cells by the rat elastase 1 (Ela1 or E1) upstream control region.
Tg(MMTV-neu/OT-I/OT-II)CBnel	007962 Under Development for Production	B6.FVB-Tg(MMTV-neu/OT-I/OT-II)CBnel Tg(Trp53R172H)8512Jmr/J
Approximately 85% of the compound mutant females develop focal mammary tumors at 6-10 months of age. Both virgin and breeder mice develop tumors. Approximately 37% of tumor-bearing mice develop metastatic disease to the lung. High expression of neu is detected in tumor tissue while very low levels are found in lung and ovary. Female mice carrying only the neu^OT-I/OT-II mutation develop focal mammary tumors at approximately 18 months of age.
Tg(Trp53R172H)8512Jmr	007962 Under Development for Production	B6.FVB-Tg(MMTV-neu/OT-I/OT-II)CBnel Tg(Trp53R172H)8512Jmr/J
Approximately 85% of the compound mutant females develop focal mammary tumors at 6-10 months of age. Both virgin and breeder mice develop tumors. Approximately 37% of tumor-bearing mice develop metastatic disease to the lung. High expression of neu is detected in tumor tissue while very low levels are found in lung and ovary. Female mice carrying only the neu^OT-I/OT-II mutation develop focal mammary tumors at approximately 18 months of age.

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