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J Biol Chem, Vol. 274, Issue 45, 31981-31986, November 5, 1999
From the Department of Urology, University of Texas Southwestern
Medical Center, Dallas, Texas 75235-9110
DOC-2/DAB2, a novel phosphoprotein with
signal-transducing capability, inhibits human prostatic cancer cells
(Tseng, C.-P., Ely, B. D., Li, Y., Pong, R.-C., and Hsieh, J.-T.
(1998) Endocrinology 139, 3542-3553). However, its
mechanism of action is not understood completely. This study delineates
the functional significance of DOC-2/DAB2 protein phosphorylation and
demonstrates that in vivo activation of protein kinase C
(PKC) by 12-O-tetradecanoylphorbol-13-acetate (TPA) induces
DOC-2/DAB2 phosphorylation, including a serine residue at position 24. Mutation of Ser24 to Ala reduced DOC-2/DAB2 phosphorylation
by PKC. Using a synthetic Ser24 peptide
(APS24KKEKKKGSEKTD) or recombinant DOC-2/DAB2 as
substrates, PKC
II, PKC
, and PKC
(but not casein kinase II)
directly phosphorylated Ser24 in vitro. This
indicates that DOC-2/DAB2 is a PKC-specific substrate. Since expression
of wild-type DOC-2/DAB2, but not the S24A mutant, inhibited TPA-induced
AP-1 activity in prostatic epithelial cells, phosphorylation of
Ser24 appears to play a critical role in modulating
TPA-induced AP-1 activity. Taken together, these data suggest that
PKC-regulated phosphorylation of DOC-2/DAB2 protein may help its growth
inhibitory function.
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