Sentence examples for still activate from inspiring English sources

This is supported by our observation that PINK1-induced phosphorylation of Parkin can still activate E3 ligase activity in the presence of S65A ubiquitin as judged by Miro1 ubiquitylation and this is abolished by the Parkin S65A mutant.

The RIN1 GEF domain mutant RIN1E574A, which cannot activate RAB5 but can still activate ABL, suppressed RAB5 activity in a dominant negative manner and blocked EGFR degradation while it promoted receptor recycling.

Since reduced-activity mutants could still activate MEK/ERK via CRAF [ 11, 13, 14], demonstration of mutant-induced MEK or ERK phosphorylation in cell culture systems without evidence of inhibition of mutant-induced MEK or ERK phosphorylation by BRAF inhibitors was not sufficient to define a kinase-activated mutant.

It was further demonstrated that additional mutation of K708 prevented the activation by AITC but THC could still activate the channel.

However, when the cysteine residues were mutated, the activation by NMM was abolished, but THC and WIN55,212-2 could still activate the channel possibly by binding to a site.

Since kinase-inactive EGFRvIII is still able to be an activator for a partner receptor, inhibitor-bound-EGFRvIII may still activate other receptors of the EGFR family (ERBB2 or ERBB4).

For example, the active site inhibitor KU63794 blocks mTOR and dampens the negative feedback loop leading to Akt activation, but still activates Erks in Panc1 cells (37).

In agreement with the computed MISs, ERK1/2 is deactivated in the case of H. pylori stimulation, but is still activated in the case of HGF activation, demonstrating the different response of the network for the two stimuli.

Our interpretation of these data is that each of the new hLCB2a mutants had a small impact on SPT activity and that each mutant enzyme is still activated by the presence of the activating small subunits.

RIN1QM, a mutant that cannot activate ABL but still activates RAB5, caused dominant suppression of EGF-induced ABL kinase activation and accelerated EGFR degradation.

However, in the presence of caspase-8 inhibitor, PR8 infection still activated caspase-9, suggesting it to be independent of caspase-8 activation (Supplementary Figure S3).