Title : Glycogen synthase kinase-3β is a crucial mediator of signal-induced RelB degradation.

Pub. Date : 2011 May 26

PMID : 21217772






3 Functional Relationships(s)
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1 In Jurkat leukaemic T cells as well as in primary human T cells, tetradecanoylphorbolacetate/ionomycin- and CD3/CD28-induced RelB degradation were impaired by a GSK-3beta-specific pharmacological inhibitor, an ectopically expressed dominant-negative GSK-3beta mutant and by small-interfering RNA-mediated silencing of GSK-3beta expression. Tetradecanoylphorbol Acetate glycogen synthase kinase 3 beta Homo sapiens
2 In Jurkat leukaemic T cells as well as in primary human T cells, tetradecanoylphorbolacetate/ionomycin- and CD3/CD28-induced RelB degradation were impaired by a GSK-3beta-specific pharmacological inhibitor, an ectopically expressed dominant-negative GSK-3beta mutant and by small-interfering RNA-mediated silencing of GSK-3beta expression. Tetradecanoylphorbol Acetate glycogen synthase kinase 3 beta Homo sapiens
3 In Jurkat leukaemic T cells as well as in primary human T cells, tetradecanoylphorbolacetate/ionomycin- and CD3/CD28-induced RelB degradation were impaired by a GSK-3beta-specific pharmacological inhibitor, an ectopically expressed dominant-negative GSK-3beta mutant and by small-interfering RNA-mediated silencing of GSK-3beta expression. Tetradecanoylphorbol Acetate glycogen synthase kinase 3 beta Homo sapiens