Caspase-9 and caspase 3, which are downregulated upon PKB/Akt activation, fail to activate pathways leading to apoptosis [ 19].
These results suggest that STACs that fail to activate E230 mutants are direct activators of SIRT1.
The mutation of the STAT site fail to activate the chrysin induced p21 Wactivityvity, which suggests STAT response element at −692 to −684 is critical for chrysin mediated transactivation of p21 WAF1 promoter.
During T cell activation, anergic clones fail to activate ERK1/2; however, there is also evidence that inhibition of ERK1/2 alone cannot act on this unresponsive state known as clonal anergy [ 47].
This may be one explanation for why Akt is necessary for ErbB2 tumourigenesis [ 52, 53], but is not sufficient for mammary tumourigenesis [ 11, 12]: activation of Akt alone may fail to activate Erk.
We find that satellite cells are maintained in aged human skeletal muscle, but fail to activate in response to muscle attrition, due to diminished activation of Notch compounded by elevated transforming growth factor beta (TGF-β /phospho Smad3 (pSmad3).
In the presence of ethylene, the ethylene receptors fail to activate CTR1, relieving repression of EIN2 and allowing for EIN2 activation of the EIN3 family of transcription factors (Kendrick and Chang 2008).
We speculate that in the absence of aPKC activity, cells that downregulate NANOG and maintain GATA6, but fail to activate GATA4, may also undergo cell death.
In contrast, cisplatin-resistant cells fail to activate caspase-8 via this pathway despite conserving sensitivity to death ligand-driven activation.
We show that Lkb1-deficient larvae fail to activate autophagy in response to nutrient restriction.
However, most studies agree that monomers fail to activate Factor C.
