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A New Model System for Studying the Phosphatidylinositol Cycle

Overview
Journal J Cell Physiol
Specialties Cell Biology
Physiology
Date 1982 Jul 1
PMID 7050132
Citations 4
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Abstract

An early manifestation of the response of WRK-1 rat mammary tumor cells to vasopressin is an increase in incorporation of (32P)Pi into phospholipids. Incorporation into all classes of phospholipids is stimulated; however, incorporation into phosphatidylinositol (PI) is increased to the greatest degree (3- to 10-fold as compared with 1.3- to 2-fold for the other phospholipids). Furthermore, increased incorporation into PI is accompanied by an increased rate of PI turnover; turnover rates of the other phospholipids are unaffected by vasopressin.

Citing Articles

Stimulation, by vasopressin and other agonists, of inositol-lipid breakdown and inositol phosphate accumulation in WRK 1 cells.

Kirk C, Guillon G, Balestre M, Jard S Biochem J. 1986; 240(1):197-204.

PMID: 3827839 PMC: 1147393. DOI: 10.1042/bj2400197.


Phorbol ester inhibition of the hormone-stimulated phosphoinositide cycle in WRK-1 cells.

Monaco M, Mufson R Biochem J. 1986; 236(1):171-5.

PMID: 3790069 PMC: 1146802. DOI: 10.1042/bj2360171.


Characterization of specific V1a vasopressin-binding sites on a rat mammary-tumour-cell line.

Guillon G, Kirk C, Balestre M Biochem J. 1986; 240(1):189-96.

PMID: 3030277 PMC: 1147392. DOI: 10.1042/bj2400189.


Effect of dual agonists on phosphoinositide pools in WRK-1 cells.

Monaco M, Attinasi M, Koreh K Biochem J. 1990; 269(3):633-7.

PMID: 2167661 PMC: 1131634. DOI: 10.1042/bj2690633.