Inhibitory regulation of phospholipase C-β1 by a G protein dependent mechanism

I. Litosch

Research output: Contribution to journalArticle

Abstract

Rat liver plasma membranes reconstituted with bovine brain PLCβ, exhibit a dual regulation of PLC-β, activity by G proteins. Low concentrations of GTP-γ-S inhibited PLC-β, activity while high concentrations of GTP-γ-S stimulated PLC-β, activity. In the presence of GTP, the α2-selective adrenergic agonists, clonidine and oxymethazoline, inhibited PLC-β1 activity. The aminosteroid U-73122 blocked PLC-β1 inhibition by GTP plus clonidine and the stimulation due to GTP-γ-S plus vasopressin. αo/iGDP attenuated the GTP-γ-S dependent inhibition of PLC-β, while αo/iGTP-γ-S had no effect suggesting an involvement of G protein βγ subunits in the inhibitory mechanism. Low concentrations of βγ subunits inhibited PLC-β1 activity. Inhibition was followed by reversal to basal and onset of stimulation as the βγ concentration was increased. Inhibition by βγ was dependent on the presence of membranes. Treatment of membranes with anti-αq/11 antibody attenuated the βγ inhibition. These results indicate that the rapid and transient inhibition of PLC-β1 which occurs at low ligand concentrations may be mediated through βγ subunits and occurs through a mechanism which is dependent on αq.

Original languageEnglish
JournalFASEB Journal
Volume10
Issue number6
StatePublished - Dec 1 1996
Externally publishedYes

Fingerprint

clonidine
phospholipase C
Type C Phospholipases
Programmable logic controllers
Guanosine Triphosphate
G-proteins
GTP-Binding Proteins
adrenergic agonists
vasopressin
protein subunits
plasma membrane
Clonidine
brain
liver
antibodies
cattle
rats
Adrenergic Agonists
Membranes
Protein Subunits

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

Inhibitory regulation of phospholipase C-β1 by a G protein dependent mechanism. / Litosch, I.

In: FASEB Journal, Vol. 10, No. 6, 01.12.1996.

Research output: Contribution to journalArticle

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