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It was shown previously that the sequence CTAATTG is critical for Xvent-2B binding, and that the binding is enhanced by the presence of an additional ATTA motif six or seven nucleotides 3' of the core TAAT [6].
The binding is enhanced by additional hydrophobic interactions of the aromatic side-chain of Phe4.
This binding is enhanced by Pat-C and inhibited by the P-rich region.
DCP2 and EDC4 binding is enhanced by the P-rich region and does not require LSm1 7.
For RCA, binding is enhanced by 2- O- or 6- O-sulfation but abolished by 4- O-sulfation (41).
Cytoplasmic p27 increases cell motility by RhoA inhibition, disrupting actin cytoskeletal stability [ 16]. p27-RhoA binding is enhanced by p27 phosphorylation at T198 [ 14].
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In turn, RhoA membrane binding was enhanced by 1.7-fold (Fig 6B).
We found that cell surface expression of M3RTP/LP, as detected by [H]NMS binding, was enhanced by incubation with each antagonist utilized in this study.
We found that Plx1 co-precipitated with Mcm7 and that its binding was enhanced by activation of the checkpoint induced by pApT.
Similar to RASSF1A, RASSF6 could co-immunoprecipitate with MAP-1 and this binding was enhanced by the presence of activated K-Ras (suggesting a potential mechanism by which Ras may activate the pro-apoptotic effects of RASSF6) [198].
However, since we found that collagen binding was enhanced by DDR1 over-expression we determined whether the activation and recruitment of β1 integrins, and the enrichment of focal adhesions with the actin binding proteins talin, paxillin and vinculin, would be influenced.
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