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Title: Steady-state levels of G-protein beta-subunit expression are regulated by treatment of cells with bacterial toxins

Abstract

Cultures of 3T3-L1 cells were incubated with either 10 ng/ml cholera toxin or 10 ng/ml pertussis toxin from 4 days prior to the initiation of differentiation and throughout the subsequent incubation. Toxin concentrations were sufficient to completely prevent the labelling of alpha-subunits with (/sup 32/P)NAD/sup +/ and pertussis toxin and to prevent by more than 90% the labelling with (/sup 32/P)NAD/sup +/ and cholera toxin in membranes prepared from these cells. Neither toxin prevented the differentiation to the adipocyte phenotype. Neither toxin prevented the increases in the relative amounts of G-proteins which occur upon differentiation. Both toxins dramatically decreased the amount of beta-subunits. As measured by quantitative immunoblotting with antisera specific for both the 35 kDa and 36 kDa beta-subunits, levels of beta-subunit were decreased by more than 50% of steady-state level of control cells. Thus, bacterial toxins which modifies G-protein alpha-subunits are capable of modulating the levels of beta-subunits in vivo. The basis for the regulation of G-protein subunit expression by bacterial toxins is under study.

Authors:
; ;
Publication Date:
Research Org.:
State Univ. of New York, Stony Brook
OSTI Identifier:
6024235
Report Number(s):
CONF-870644-
Journal ID: CODEN: FEPRA; TRN: 87-033996
Resource Type:
Conference
Resource Relation:
Journal Name: Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States); Journal Volume: 46:6; Conference: 78. annual meeting of the American Society of Biological Chemists conference, Philadelphia, PA, USA, 7 Jun 1987
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES; FIBROBLASTS; CELL DIFFERENTIATION; PROTEINS; BIOSYNTHESIS; LABELLING; TOXINS; BIOLOGICAL EFFECTS; BACTERIA; FAT CELLS; NAD; PHOSPHORUS 32; STEADY-STATE CONDITIONS; TRACER TECHNIQUES; ANIMAL CELLS; ANTIGENS; BETA DECAY RADIOISOTOPES; BETA-MINUS DECAY RADIOISOTOPES; COENZYMES; CONNECTIVE TISSUE CELLS; DAYS LIVING RADIOISOTOPES; ISOTOPE APPLICATIONS; ISOTOPES; LIGHT NUCLEI; MATERIALS; MICROORGANISMS; NUCLEI; NUCLEOTIDES; ODD-ODD NUCLEI; ORGANIC COMPOUNDS; PHOSPHORUS ISOTOPES; RADIOISOTOPES; SOMATIC CELLS; SYNTHESIS; TOXIC MATERIALS; 550201* - Biochemistry- Tracer Techniques

Citation Formats

Watkins, D.C., Northup, J.K., and Malbon, C.C. Steady-state levels of G-protein beta-subunit expression are regulated by treatment of cells with bacterial toxins. United States: N. p., 1987. Web.
Watkins, D.C., Northup, J.K., & Malbon, C.C. Steady-state levels of G-protein beta-subunit expression are regulated by treatment of cells with bacterial toxins. United States.
Watkins, D.C., Northup, J.K., and Malbon, C.C. 1987. "Steady-state levels of G-protein beta-subunit expression are regulated by treatment of cells with bacterial toxins". United States. doi:.
@article{osti_6024235,
title = {Steady-state levels of G-protein beta-subunit expression are regulated by treatment of cells with bacterial toxins},
author = {Watkins, D.C. and Northup, J.K. and Malbon, C.C.},
abstractNote = {Cultures of 3T3-L1 cells were incubated with either 10 ng/ml cholera toxin or 10 ng/ml pertussis toxin from 4 days prior to the initiation of differentiation and throughout the subsequent incubation. Toxin concentrations were sufficient to completely prevent the labelling of alpha-subunits with (/sup 32/P)NAD/sup +/ and pertussis toxin and to prevent by more than 90% the labelling with (/sup 32/P)NAD/sup +/ and cholera toxin in membranes prepared from these cells. Neither toxin prevented the differentiation to the adipocyte phenotype. Neither toxin prevented the increases in the relative amounts of G-proteins which occur upon differentiation. Both toxins dramatically decreased the amount of beta-subunits. As measured by quantitative immunoblotting with antisera specific for both the 35 kDa and 36 kDa beta-subunits, levels of beta-subunit were decreased by more than 50% of steady-state level of control cells. Thus, bacterial toxins which modifies G-protein alpha-subunits are capable of modulating the levels of beta-subunits in vivo. The basis for the regulation of G-protein subunit expression by bacterial toxins is under study.},
doi = {},
journal = {Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States)},
number = ,
volume = 46:6,
place = {United States},
year = 1987,
month = 5
}

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