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KMID : 0624620120450050287
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BMB Reports
2012 Volume.45 No. 5 p.287 ~ p.292
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FGF-2 inhibits TNF-α mediated apoptosis through upregulation of Bcl2-A1 and Bcl-xL in ATDC5 cells
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Kim Hey-Ryun
Heo Youn-Moo
Jeong Kyoung-Il
Kim Yong-Min
Jang Hae-Lan
Lee Kwang-Yeol
Yeo Chang-Yeol
Kim Sung-Hoon
Lee Hak-Kyo
Kim Seung-Ryul
Kim Eung-Gook
Choi Joong-Kook
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Abstract
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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.
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KEYWORD
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Apoptosis, ATDC5 cells, Bcl-xL, Bcl2-A1, FGF-2, TNF-α
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