Title : Insulin receptor autophosphorylation sites tyrosines 1162 and 1163 control both insulin-dependent and insulin-independent receptor internalization pathways.

Pub. Date : 1994 Jan

PMID : 8011427






1 Functional Relationships(s)
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1 We show here that (1) in CHO-Y2 cells, basal endocytosis, like insulin-induced internalization, was markedly altered despite normal receptor turnover and (2) in both CHO-R and CHO-Y2 cells, basal receptor endocytosis was altered by tunicamycin, an inhibitor of protein N-glycosylation, whereas insulin-induced internalization was not. Tunicamycin insulin Cricetulus griseus