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FRNK, the autonomously expressed C‐terminal region of focal adhesion kinase, is uniquely regulated in vascular smooth muscle: Analysis of expression in transgenic mice
Author(s) -
Hayasaka Haruko,
Simon Kate,
Hershey E. Daniel,
Masumoto Kohhei,
Parsons J. Thomas
Publication year - 2005
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20501
Subject(s) - biology , genetically modified mouse , vascular smooth muscle , enhancer , transgene , microbiology and biotechnology , ectopic expression , focal adhesion , promoter , gene expression , gene , signal transduction , endocrinology , biochemistry , smooth muscle
FRNK, the autonomously expressed carboxyl‐terminal region of focal adhesion kinase (FAK), is expressed in tissues that are rich in vascular smooth muscle cells (VSMCs). Here we report the generation of transgenic mice harboring the putative FRNK promoter fused to LacZ and examine the promoter activity in situ via expression of β‐galactosidase. The transgenic mice exhibited expression of β‐galactosidase predominantly in arterial VSMCs in large and small blood vessels of major organs. Upregulation of β‐galactosidase activity was observed in tunica media following carotid injury, indicating that the FRNK promoter is activated in VSMCs in response to injury. Robust expression of β‐galactosidase in blood vessels was also detected in the developing embryo. However, expression was also observed in the midline, the nose and skin epidermis, indicating distinct transcriptional regulation of the FRNK promoter in embryogenesis. To analyze FRNK expression in vitro, we identified a 116 bp sequence in the FRNK promoter that was sufficient to function as an enhancer when fused to the minimal actin promoter and expressed in cultured smooth muscle cells. Mutation of AP‐1 and NF‐E2 binding consensus sequences within this element abrogated enhancer activity, supporting the involvement of this promoter element in VSMC expression of FRNK. © 2005 Wiley‐Liss, Inc.