期刊
BMC DEVELOPMENTAL BIOLOGY
卷 16, 期 -, 页码 -出版社
BMC
DOI: 10.1186/s12861-016-0135-8
关键词
NF-kB; RelA; p65; Flox; Tamoxifen; Cre; Col1a2
资金
- UTMB CTSA [UL1TR001439]
- NIEHS [P30 ES006676]
- AHA [13GRNT17120070]
- [F30HL128036]
- [PO1 AI068865]
Background: Nuclear Factor-Kappa B (NF-kB) is a family of transcription factors that are important in embryonic development, inflammation, epithelial-to-mesenchymal transition and cancer. The 65 kDa RelA subunit is the major transcriptional activator of the NF-kB pathways. Whole-body deficiency of RelA leads to massive apoptosis of liver hepatocytes and death in utero. To study the role of RelA in physiology and in disease states in a manner that circumvents this embryonic lethal phenotype, we have generated a mouse with RelA conditional knockout (CKO) alleles containing loxP sites that are deleted by activated Cre recombinase. Results: We demonstrate that RelA(CKO/CKO) mice are fertile, do not display any developmental defects and can be crossed with Cre-expressing mice to delete RelA in a temporal, tissue-specific manner. Our mating of RelA(CKO/CKO) mice with Zp3-Cre transgenic led to embryonic lethality of RelA-deficient embryos. In contrast, mating of RelA(CKO/CKO) mice with Col1 alpha 2-CreER mice allowed for the generation of double transgenics which could be stimulated with tamoxifen to induce fibroblast-specific RelA deletion in adulthood. Conclusions: Based on our collective data, we conclude that this novel RelA(CKO/CKO) mouse allows for efficient deletion of RelA in a tissue-specific manner. This RelA(CKO/CKO) mouse will be an invaluable tool for deciphering the mechanistic roles of RelA in various cells and tissues during development and in disease.
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