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Activation of protein kinase C inhibits prostaglandin‐ and potentiates adenosine receptor‐stimulated accumulation of cyclic AMP in a human T‐cell leukemia line
Author(s) -
Nordstedt Christer,
Jondal Mikael,
Fredholm Bertil B.
Publication year - 1987
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(87)80875-x
Subject(s) - forskolin , adenosine , endocrinology , medicine , protein kinase c , prostaglandin e2 , protein kinase a , prostaglandin , receptor , phorbol , jurkat cells , chemistry , cell culture , adenosine receptor , biology , signal transduction , kinase , biochemistry , t cell , immunology , agonist , immune system , genetics
Accumulation of cAMP in the human T‐cell leukemia cell line Jurkat was stimulated by the adenosine analogue 5′‐ N ‐ethylcarboxamidoadenosine (NECA) and by prostaglandin E 2 , (PGE 2 ). Addition of two phorbol esters, PDiBu and TPA, markedly enhanced the NECA‐stimulated accumulation of cAMP whereas the PGE 2 ‐stimulated cAMP accumulation was substantially reduced. The non‐tumor‐promoting phorbol ester, 4α‐PDD, had no effect on either NECA‐ or PGE 2 ‐stimulated cAMP accumulation. The ability of PDiBu to inhibit the effect of PGE 2 and to stimulate the effect of NECA remained in the presence a low concentration of forskolin (0.3 μM), which per se increased both NECA‐ and PGE 2 ‐stimulated cAMP accumulation. Our results suggest that the effect of PK‐C‐activating drugs on receptor‐mediated cAMP accumulation is entirely dependent on which receptor is being stimulated

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