WRK-1 rat mammary tumour cells respond to vasopressin with increased accumulation of inositol phosphates as well as increased precursor incorporation into phosphatidylinositol. The phorbol ester, phorbol 13-myristate 12-acetate (PMA) inhibits by 80% both inositol phosphate accumulation and increased precursor incorporation. This inhibition is much less evident at early times (2 min) than at later times (25 min). The vasopressin-induced rise in cytosolic free Ca2+ is inhibited in a similar manner. Oleoylacetylglycerol is inactive with respect to inhibition of vasopressin-induced increases in incorporation of 32P into phosphoinositides. PMA has no effect on vasopressin binding at saturating concentrations of the hormone and does not affect the binding affinity.
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May 1986
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Research Article|
May 15 1986
Phorbol ester inhibition of the hormone-stimulated phosphoinositide cycle in WRK-1 cells Available to Purchase
Publisher: Portland Press Ltd
Online ISSN: 1470-8728
Print ISSN: 0264-6021
© 1986 London: The Biochemical Society
1986
Biochem J (1986) 236 (1): 171–175.
Citation
M E Monaco, R A Mufson; Phorbol ester inhibition of the hormone-stimulated phosphoinositide cycle in WRK-1 cells. Biochem J 15 May 1986; 236 (1): 171–175. doi: https://doi.org/10.1042/bj2360171
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