Generation of mice with a conditional Stat1 null allele

被引:26
作者
Wallner, Barbara [1 ]
Leitner, Nicole R. [1 ]
Vielnascher, Raimund M. [1 ]
Kernbauer, Elisabeth [2 ]
Kolbe, Thomas [3 ,4 ]
Karaghiosoff, Marina [1 ]
Ruelicke, Thomas [3 ,5 ]
Decker, Thomas [2 ]
Mueller, Mathias [1 ,3 ]
机构
[1] Univ Vet Med, Inst Anim Breeding & Genet, A-1210 Vienna, Austria
[2] Univ Vienna, Dept Genet Microbiol & Immunobiol, Max F Perutz Labs, A-1030 Vienna, Austria
[3] Univ Vet Med, Univ Ctr Biomodels Austria BIAT, A-1210 Vienna, Austria
[4] Univ Nat Resources & Appl Life Sci, Dept IFA Tulln, A-3430 Tulln, Austria
[5] Univ Vet Med, Inst Lab Anim Sci, A-1210 Vienna, Austria
基金
奥地利科学基金会;
关键词
Stat1; Conditional knockout; Cre recombinase; Interferon; TARGETED DISRUPTION; IFN-GAMMA; GENE; IMMUNITY; LAMBDA; ROLES;
D O I
10.1007/s11248-011-9519-5
中图分类号
Q5 [生物化学];
学科分类号
071010 ; 081704 ;
摘要
Interferons (IFNs) are key cytokines in the innate immune response that also bridge the gap to adaptive immunity. Signaling upon stimulation by IFN type I, II and III is mediated by the Jak-Stat pathway. STAT1 is activated by all three IFN receptor complexes and absence of STAT1 from mice increases their susceptibility to pathogens. In addition, depending on the setting, STAT1 can act as tumor suppressor or oncogene. Here we report the generation and detailed functional characterization of a conditional Stat1 knockout mouse. We show the integrity of the conditional Stat1 locus and report successful in vivo deletion by means of a ubiquitous and a tissue-specific Cre recombinase. The conditional Stat1 null allele represents an important tool for identifying novel and cell-autonomous STAT1 functions in infection and cancer.
引用
收藏
页码:217 / 224
页数:8
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