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Adenosine 3′,5′‐cyclic monophosphate (cAMP) inhibits phorbol ester‐induced growth of an IL‐2‐dependent T cell line
Author(s) -
Goto Yuso,
Takeshita Toshikazu,
Sugamura Kazuo
Publication year - 1988
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(88)80909-8
Subject(s) - forskolin , cholera toxin , protein kinase c , signal transduction , cyclic adenosine monophosphate , adenosine , phorbol , second messenger system , cell culture , phorbol ester , protein kinase a , chemistry , biology , microbiology and biotechnology , biochemistry , medicine , endocrinology , enzyme , receptor , genetics
We previously established a human T cell line, TPA‐Mat, which can proliferate in response to not only interleukin‐2 (IL‐2), but also phorbol esters such as 12‐ O ‐tetradecanoylphorbol‐13‐acetate (TPA) and phorbol‐12,13‐dibutyrate (PDBu). The present study demonstrated that the PDBu‐dependent growth of TPA‐Mat cells was inhibited up to 90% by adenosine 3′,5′‐cyclic monophosphate (cAMP) raising agents such as forskolin, cholera toxin and 1‐methyl‐3‐isobutylxanthine, and cAMP analogues, whereas the IL‐2‐stimulated TPA‐Mat growth was slightly inhibited. These findings suggest that the signal transduction pathway of PDBu‐induced growth, which should involve activation of protein kinase C, is sensitive to cAMP, and that it cannot be exactly identical to the signal transduction pathway of Il‐2‐induced growth in TPA‐Mat cells.