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FGF-2 inhibits TNF-α mediated apoptosis through upregulation of Bcl2-A1 and Bcl-xL in ATDC5 cells

Title
FGF-2 inhibits TNF-α mediated apoptosis through upregulation of Bcl2-A1 and Bcl-xL in ATDC5 cells
Authors
Kim H.-R.Heo Y.-M.Jeong K.-I.Kim Y.-M.Jang H.L.Lee K.-Y.Yeo C.-Y.Kim S.H.Lee H.-K.Kim S.-R.Kim E.-G.Choi J.-K.
Ewha Authors
여창열
SCOPUS Author ID
여창열scopus
Issue Date
2012
Journal Title
BMB Reports
ISSN
1976-6696JCR Link
Citation
vol. 45, no. 5, pp. 287 - 292
Indexed
SCIE; SCOPUS; KCI WOS scopus
Abstract
FGF-2 is involved in cell survival, proliferation, apoptosis, and angiogenesis in a wide variety of cells. FRGRs, PI3K and MAP kinases are well known mediators of FGF signaling. Despite its known roles during many developmental processes, including osteogenesis, there are few known targets of FGF-2. In the present study, we identified Bcl2-A1 and Bcl-xL as two prominent targets involved in promoting cell survival. Pretreatment of ATDC5 cells with FGF-2 increased cell survival, while siRNAs specific for Bcl2-A1 and Bcl-xL compromised the anti-apoptotic effect of FGF-2, sensitized the cells to apoptosis triggered by TNF-α. Chemical inhibition of FGFR, NFkB, and PI3K activity by PD173074, pyrrolidine dithiocarbamate, and LY294002 respectively abrogated the FGF-2-mediated induction of Bcl2-A1 and Bcl-xL expression. Taken together, our data demonstrate that a subset of Bcl2 family proteins are the targets of FGF-2 signaling that promotes the survival of ATDC5 cells. © 2012 by the The Korean Society for Biochemistry and Molecular Biology.
DOI
10.5483/BMBRep.2012.45.5.287
Appears in Collections:
자연과학대학 > 생명과학전공 > Journal papers
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