Title : Identification and characterization of the nonphosphorylated precursor of pp17, a phosphoprotein associated with phorbol ester induction of growth arrest and monocytic differentiation in HL-60 promyelocytic leukemia cells.

Pub. Date : 1986 Oct 25

PMID : 3464595






4 Functional Relationships(s)
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1 Treatment of HL-60 promyelocytic leukemia cells with the tumor-promoting phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), causes rapid phosphorylation and dephosphorylation of pp17, a 17-20-kDa, pI 5.5 cytosolic protein, as an early event in a response sequence leading to growth arrest and terminal differentiation into monocytes (Feuerstein, N., and Cooper, H. L., (1984) J. Biol. Tetradecanoylphorbol Acetate stathmin 1 Homo sapiens
2 Upon TPA treatment, pre-existing p17 was rapidly phosphorylated to pp17. Tetradecanoylphorbol Acetate stathmin 1 Homo sapiens
3 Quantitatively, therefore, the phosphorylation of p17 to pp17 is one of the most prominent early biochemical responses to TPA treatment. Tetradecanoylphorbol Acetate stathmin 1 Homo sapiens
4 Available data indicate that p17 predominates in rapidly proliferating cells, while phosphorylation to pp17 occurs where cell growth is modified by TPA or other agents. Tetradecanoylphorbol Acetate stathmin 1 Homo sapiens