Title : JNK2 is activated during ER stress and promotes cell survival.

Pub. Date : 2012 Nov 22

PMID : 23171849






1 Functional Relationships(s)
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1 Here we show in U937 cells that the ER stressors tunicamycin and thapsigargin cause increased expression of c-Jun N-terminal kinase 2 (JNK2), which allows regulation of the UPR, whose silencing or pharmacological inhibition delays BiP (immunoglobulin heavy-chain binding protein) upregulation, and causes earlier and greater expression of CCAAT/enhancer-binding protein-homologous protein (CHOP). Tunicamycin heat shock protein family A (Hsp70) member 5 Homo sapiens