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Since this same mutant of CXCR2 has been shown earlier to be deficient in binding to AP-2 [19] and Hsp70 interacting protein (HIP) [18], we conclude that the I323-L324 residues of CXCR2 are required for CXCR2 binding to AP-2, HIP and LASP-1 in a spatiotemporal manner resulting in efficient and controlled chemotaxis.
HB19-1 Δp66 bacteria were previously shown to be deficient in binding to integrin αVβ3 (Coburn and Cugini, 2003).
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To extend these observations and directly investigate whether that F11-mediated inhibition of RhoA signalling promotes viral release and spread we have generated recombinant viruses lacking F11 or expressing an F11 mutant (F11-VK), which is deficient in binding RhoA [28].
The truncation mutant in desmocollin-2a is deficient in binding plakoglobin.
It is deficient in binding to RanGTP and imposes a general block on receptor-mediated NPC passage.
As a control, V-E235A, which is deficient in binding to MDA5 [ 53] (as detailed in Additional file 5), showed a minimal inhibitory effect, as expected.
WWOX L404A, which is deficient in binding to GSK3 β and was incapable of restoring Tau activity on microtubule formation, should fail to stimulate neuronal cell differentiation.
R145W has been shown to have disrupted kinase activity [ 20, 21] and I175T is deficient in binding and phosphorylation of Cdc25A and in binding to BRCA1 and p53 [ 20- 22].
Significantly, although the MTA1 and MTA2 mutant proteins with deletion of the C-terminal H3 tail binding domain were assembled into the endogenous NURD complex when expressed in mammalian cells, the resulting NURD complexes were deficient in binding H3 tail in vitro, indicating that the MTA family proteins are required for the observed specific binding of H3 tail peptide by NURD in vitro.
The MAH ΔGPL/4B2 strain with a mutation in glycopeptidolipid production is deficient in binding to human epithelial cells (HEp-2), as well as deficient in its ability to bind to and colonize the intestinal tract of C. elegans as efficiently as wild-type MAH.
Two mutations occur in exon 2 of cdk4 at the same codon (Arg24Cys, Arg24His) and functional analysis of the Arg24Cys mutant protein reveals that it is deficient in binding to p16INK4 a, but is capable of binding cyclin D and phosphorylating pRB.
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