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Tunicamycin‐mediated depletion of insulin receptors in 3T3‐L1 adipocytes
Author(s) -
Rosen O. M.,
Chia G. H.,
Fung C.,
Rubin C. S.
Publication year - 1979
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1040990106
Subject(s) - tunicamycin , cycloheximide , receptor , insulin , insulin receptor , glycosylation , medicine , hexose , endocrinology , 3t3 l1 , chemistry , biology , adipocyte , adipose tissue , protein biosynthesis , biochemistry , insulin resistance , enzyme , apoptosis , unfolded protein response
Tunicamycin, an antibiotic that inhibits protein glycosylation, elicited a rapid depletion of insulin binding activity at the surface of 3T3‐L1 adipocytes. Disappearance of insulin receptors occurred more rapidly in the presence of tunicamycin than when protein synthesis was inhibited by cycloheximide and was accompanied by a diminution in sensitivity of the adipocytes to the acute effects of insulin and anit‐insulin receptor antibody on hexose uptake and metabolism.