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Reciprocally, the VAPB double mutant (K87D M89D) that is defective in FFAT binding was unable to interact with ASNA1.
The Nup53 mutant defective in RRM dimerization, which showed reduced membrane binding, was unable to substitute for the endogenous protein in nuclear assembly.
A mutant p21 that is defective in CDK2 binding was unable to disrupt the CDK2 NF-YA interaCDK2 NF-YAuppress PLK1 transcrinteraction
An effector mutant of RhoE (Thr55Ala) defective for p190 RhoGAP binding, was unable to induce stress fibre loss (Wennerberg et al, 2003).
In contrast, the DNMT1 mutant deficient in UHRF1 binding was unable to reestablish local DNA methylation patterns resulting in decreased levels at the major satellite repeats (average 19%) similar to the Dnmt1 −/− control cell line (average 18%).
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The calcium binding ability of the C-terminal domain of F1 TnC is crucial for stretch activation: F1 TnC mutations designed to abolish calcium binding are unable to contract in an asynchronous manner (8).
The mps2-381 allele that is defective in Mps3 binding is unable to form a bridge or satellite at the non-permissive temperature, supporting the idea that Mps2 plays a role early in SPB duplication (Jaspersen et al., 2006).
Furthermore, TATA binding protein was unable to bind the TATA box of the CXCL11 promoter, suggesting that assembly of transcriptional machinery was disrupted.
Bag-1S with point mutations in the Hsc70/Hsp70 binding domain was unable to confer apoptosis protection.
Consistent with its defect in lipid binding, Q785R was unable to either tubulate or aggregate liposomes (Fig. 7A, B and D).
The point mutated EBF binding site was unable to abolish complex formation even in a 1000-fold molar excess, indicating that we detect specific protein DNA interactions with this experimental set up. 18 out of the 24 new binding sites competed for complex formation when added in a 300- or 1000-fold molar excess, and thus have the ability to bind EBF in vitro.
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