Sentence examples for mutants to activate from inspiring English sources

The ability of hNGF and hproNGFR100E mutants to activate p75NTR signaling was then evaluated in cultured rat oligodendrocyte progenitors cells (OPCs), which express the p75NTR receptor, in the absence of TrkA (Fig. 4D).

To assess the ability of TRAF6 mutants to activate TAK1, we transfected low levels of TRAF6 1-358 -Gyrase B muTRAF6 1-358 -Gyraseligomerization using the drug Coumermycin A1.

The effectiveness of hNGFR100E mutants to activate p75NTR signaling, was assessed by analyzing the phosphorylation of c-jun at residue Ser63, through the p75NTR dependent activation of the jnk kinase [44] (Fig. S2).

We also present evidence for an association between the ability of the different UBA domain mutants to activate basal NF-κB signalling and number of affected sites in 1152 PDB patients.

A similar impairment of the ability of these rhodopsin mutants to activate transducin was previously observed, because of the resulting ∼3 kcal/mol lower affinity for the Gtα tail peptide caused by the alanine substitutions in the "hydrophobic patch".

We found evidence for a relationship between the ability of different UBA domain mutants to activate NF-κB signalling in vitro and number of affected sites in vivo in 1152 PDB patients from the UK and Italy, with A427D-SQSTM1 producing the greatest level of activation (relative to wild-type) of all PDB mutants tested to date.

Interestingly, the transcript level of p53 was not obviously affected in the def hi429 mutant, which prompted us to speculate that p53 protein might be stabilized or become more active in the mutant to activate the expression of Δ113p53.

Our results are at variance with the previously shown negative effect of CDK9 S175A mutation on the GST-CTD phosphorylation [21] and also inability of CDK9 S175A mutant to activate HIV-1 transcription in vitro [30].

We performed an Electrophoretic Mobility Shift Assay (EMSA) to investigate the ability of HCP produced by wild-type EDL933 and its derivative ΔhcpA mutant to activate NF-κB and/or AP-1 in polarized HT-29 cells when incubated for 1 and 3 h.

The ability of the PDZ mutant to activate a Hes1 luciferase reporter is substantially higher than that of wild-type Dll1 [ 40 ].

The reduced capacity of the IRAK-M CTD-∆ mutant to activate NF-κB was associated with an almost complete loss of IL-8 production.