Literature DB >> 7050132

A new model system for studying the phosphatidylinositol cycle.

M E Monaco, M E Lippman.   

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.

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Year:  1982        PMID: 7050132     DOI: 10.1002/jcp.1041120122

Source DB:  PubMed          Journal:  J Cell Physiol        ISSN: 0021-9541            Impact factor:   6.384


  4 in total

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

Authors:  G Guillon; C J Kirk; M N Balestre
Journal:  Biochem J       Date:  1986-11-15       Impact factor: 3.857

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

Authors:  M E Monaco; M Attinasi; K Koréh
Journal:  Biochem J       Date:  1990-08-01       Impact factor: 3.857

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

Authors:  M E Monaco; R A Mufson
Journal:  Biochem J       Date:  1986-05-15       Impact factor: 3.857

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

Authors:  C J Kirk; G Guillon; M N Balestre; S Jard
Journal:  Biochem J       Date:  1986-11-15       Impact factor: 3.857

  4 in total

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