Title : Akt-1 mediates survival of chondrocytes from endoplasmic reticulum-induced stress.

Pub. Date : 2010 Mar

PMID : 20020442






2 Functional Relationships(s)
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1 Interestingly, in thapsigargin and tunicamycin-stressed chondrocytes induction of the proapoptotic transcription factor CHOP preceded that of the anti-apoptotic BiP by 12 h. Although both of these agents caused sustained Akt and ERK phosphorylation; inhibition of Akt phosphorylation sensitized chondrocytes to ER stress, while blocking ERK signaling by U0126 had no effect. Tunicamycin AKT serine/threonine kinase 1 Homo sapiens
2 Interestingly, in thapsigargin and tunicamycin-stressed chondrocytes induction of the proapoptotic transcription factor CHOP preceded that of the anti-apoptotic BiP by 12 h. Although both of these agents caused sustained Akt and ERK phosphorylation; inhibition of Akt phosphorylation sensitized chondrocytes to ER stress, while blocking ERK signaling by U0126 had no effect. Tunicamycin AKT serine/threonine kinase 1 Homo sapiens