期刊
GENESIS
卷 45, 期 1, 页码 44-50出版社
WILEY
DOI: 10.1002/dvg.20261
关键词
chondrocyte; Cre-mediated recombination; conditional knockout; tamoxifen; X-Gal staining
资金
- NIAMS NIH HHS [R01 AR051189-02, K02 AR052411, K02 AR052411-01A2, R01 AR054465, R01 AR051189, R01 AR051469-03, R01 AR051469, R01 AR054465-01, R01 AR051189-03] Funding Source: Medline
Postnatal cartilage development and growth are regulated by key growth factors and signaling molecules. To fully understand the function of these regulators, an inducible and chondrocyte-specific gene deletion system needs to be established to circumvent the perinatal lethality. In this report, we have generated a transgenic mouse model (Col2a1-CreER(T2)) in which expression of the Cre recombinase is driven by the chondrocyte-specific col2a1 promoter in a tamoxifen-inducible manner. To determine the specificity and efficiency of the Cre recombination, we have bred Col2a1-CreER(T2) mice with Rosa26R reporter mice. The X-Gal staining showed that the Cre recombination is specifically achieved in cartilage tissues with tamoxifen-induction. In vitro experiments of chondrocyte cell culture also demonstrate the 4-hydroxy tamoxifen-induced Cre recombination. These results demonstrate that Col2a1-CreER(T2) transgenic mice can be used as a valuable tool for an inducible and chondrocyte-specific gene deletion approach.
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