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Binding of CDK9 to TRAF2
Author(s) -
MacLachlan Timothy K.,
Sang Nianli,
De Luca Antonio,
Puri Pier Lorenzo,
Levrero Massimo,
Giordano Antonio
Publication year - 1998
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/(sici)1097-4644(19981215)71:4<467::aid-jcb2>3.0.co;2-g
Subject(s) - microbiology and biotechnology , traf2 , kinase , biology , myogenesis , embryonic stem cell , signal transduction , tumor necrosis factor alpha , tumor necrosis factor receptor , genetics , immunology , myocyte , gene
CDK9 has been recently shown to have increased kinase activity in differentiated cells in culture and a differentiated tissue‐specific expression in the developing mouse. In order to identify factors that contribute to CDK9's differentiation‐specific function, we screened a mouse embryonic library in the yeast two‐hybrid system and found a tumor necrosis factor signal transducer, TRAF2, to be an interacting protein. CDK9 interacts with a conserved domain in the TRAF‐C region of TRAF2, a motif that is known to bind other kinases involved in TRAF‐mediated signaling. Endogenous interaction between the two proteins appears to be specific to differentiated tissue. TRAF2‐mediated signaling may incorporate additional kinases to signal cell survival in myotubes, a cell type that is severely affected in TRAF2 knockout mice. J. Cell. Biochem. 71:467–478, 1998. © 1998 Wiley‐Liss, Inc.