Sentence examples for binding failed from inspiring English sources

Kvβ2 mutants with disrupted either Kv1.2-Kvβ2 binding or Kvβ2-EB1 binding failed to increase the velocity of YFP-Kv1.2 puncta, confirming a central role of Kvβ2.

Given that lack of Ras PI3K binding failed to localize PI3K in the endosomes (Figure S1A, B), Ras plays a determining role in the virus-induced, transient activation of PI3K in the endosomes.

In line with its HP1 α-binding mediated activity, the PRR14 mutant defective in HP1 α binding failed to induce a similar effect.

We have previously observed depletion of H3K27 me3 at multiple loci in response to EtOH exposure; however, ChIP analysis of EZH2 binding failed to identify significant changes in PRC2 localization [ 10].

In spite of the large difference in genomic occupancy, detailed analysis of genes associated with GATA3 binding failed to identify any major functional differences between binding profiles in T47D and MCF7 cell lines (Additional file 1: Figure S6-S10).

Similarly, a FAK mutant at tyrosine 397, deficient for c-src binding, fails to induce focal adhesion disassembly in FAK-deficient fibroblasts [5] [7].

We show here that Sgol2 defective in PP2A binding fails to protect centromeric cohesin, as found for Sgo1 in yeast (Xu et al., 2009).

Consequently, its binding fails to induce the formation of the TLR4-MD-2-LPS heterodimer and the associated downstream signal transduction (Kim et al., 2007).

In budding yeast, mutant proteins defective specifically in PP2A binding fail to confer protection of centromeric cohesion during meiosis I (Xu et al., 2009).

LRP6 receptor mutant (S1579A), deficient in CK2-mediated phosphorylation and Dab2 binding, fails to associate with clathrin, and thus escapes the inhibitory effects of Dab2 on Wnt/β-catenin signalling.

The significance of this indirect recruitment is underscored by the observation that a c-Met receptor mutant selectively defective in Grb2 binding fails to induce branching morphogenesis in the Madin-Darby canine kidney (MDCK) cell line model system [ 34] and by the non-viable phenotype of knock-in mice expressing a Grb2 binding-deficient Gab1 mutant [ 32].