期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 102, 期 4, 页码 947-954出版社
WILEY
DOI: 10.1002/jcb.21329
关键词
gene expression; cell adhesion; vascular smooth muscle cells
资金
- NCI NIH HHS [CA 80606, CA40042] Funding Source: Medline
FRNK, a non-catalytic variant of focal adhesion kinase (FAK), is expressed in major blood vessels throughout mouse development and is postulated to play a role in regulating cell adhesion and signaling in vascular smooth muscle cells (VSMCS). The FRNK transcriptional start site lies within an intron of the FAK gene, suggesting that the FRNK gene is a gene within a gene. Here, we identified a 1kb intronic sequence of the FAK gene that is necessary for endogenous FRNK expression. Deletion of this sequence in gene-targeted mice abolished FRNK expression, showing the direct involvement of the FAK intron in the regulation of FRNK expression. The level of FAK expression was normal in the FRNK-deficient mice, indicating that FAK and FRNK are transcriptionally regulated by distinct promoters. The FRNK-deficient mice were viable, fertile, and displayed no obvious histological abnormalities in any of the major blood vessels. Western blot analysis showed that FRNK-deficientand wild-type (WT) cells had comparable levelsof steady-state and adhesion -dependent FAK autophosphorylation. Despite the fact that ectopic expression of FRNK suppresses focal adhesion formation in cultured cells, these results suggest that endogenous FRNK is not essential for development or the formation of the mouse vasculature.
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