CDK9 has been recently shown to have increased kinase activity in diff
erentiated cells in culture and a differentiated tissue-specific expre
ssion in the developing mouse. In order to identify factors that contr
ibute to CDK9's differentiation-specific function, we screened a mouse
embryonic library in the yeast two-hybrid system and found a tumor ne
crosis 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 inc
orporate additional kinases to signal cell survival in myotubes, a cel
l type that is severely affected in TRAF2 knockout mice. (C) 1998 Wile
y-Liss, Inc.