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Adenylate cyclase activity of NIH 3T3 cells morphologically transformed by ras genes
Author(s) -
Levitzki Alexander,
Rudick Joyce,
Pastan Ira,
Vass William C.,
Lowy Douglas R.
Publication year - 1986
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(86)80313-1
Subject(s) - adenylate kinase , cyclase , 3t3 cells , gene product , cell culture , biology , microbiology and biotechnology , chemistry , gene , receptor , biochemistry , gene expression , transfection , genetics
The observed homology between G‐proteins which regulate adenylate cyclase and ras proteins and the suggested role of ras in the regulation of adenylate cyclase in yeast prompted us to examine the regulation of adenylate cyclase in three cell lines: (i) NIH 3T3 cells, (ii) NIH 3T3 cells transformed by high levels of the normal ras H gene product and (iii) NIH 3T3 cells transformed by a mutated ras H gene product. We found that the regulation of adenylate cyclase by G‐proteins is identical in the three cell lines, although the response of the transformed NIH 3T3 cells to agonists is strongly attenuated. Our data suggest that mammalian ras products do not interact directly with adenylate cyclase, although their increased expression may indirectly inhibit the interaction of adenylate cyclase stimulatory receptors with G‐proteins.