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Additionally, this mutation promotes a reorientation of the side chains of K141 and E210, resulting in a weakening of the H-bond between H160 and E210 (which should decrease the anionic character of the proximal His and increase E°′) as seen in the X-ray structure.
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Molecular characterization of the tagged gene demonstrated that it corresponded to the previously reported TOMATO AGAMOUS-LIKE 1 (TAgene gene, the tomato ortholog of SHATTERPROOF MADS-box genes of Arabidopsis thaliana, and that the Alq mutation promoted a gain-of-function phenotype caused by the ectopic expression of TAGL1.
It is somewhat surprising that genetic alterations downstream of the lit/lit mutation promote a larger lifespan increase than that observed in little mice.
The mutations promote a focused and enhanced immune response [3], [49], [50] that may be particularly important in the event of an outbreak where specificity is the key to epidemic control.
In particular, the electrostatic surface potential of the ACVR1 GS domain is predicted to be appreciably affected by these disparate point mutations, promoting a shift in the equilibrium between the inactive and active ACVR1 structures causing mild kinase activation.
Comparisons between these structures revealed that beneficial mutations promoted a more compact conformation that was favorable for catalysis.
Since high Aβ43 and Aβ42 (substrates in this cycle) accumulate in vitro or are released in vivo, we speculate that FAD PSEN mutations promote a premature release of the Aβ43/Aβ42 peptides.
Further support is provided by Matthews et al. [ 102] who report that the TPO receptor TMDs self-associate, and that cysteine crosslinking revealed a TMD interaction interface, whereas the S505N mutation promotes the formation of a different dimerization interface, implying that activation involves a subunit rotation.
This led to a hypothesis that the DNM2-S619L mutation promotes defective membrane tubulation, which was tested using an in vitro tubulation assay.
This mutation promotes p185/neu homo- and heterodimerization and transforms the HER2/ neu protooncogene into a dominant transforming oncogene.
A recent investigation into the role of EZH2 suggests that the latter may apply; EZH2 hotspot mutation promotes the accumulation of GCB cells and EHZ2 inhibition promotes transition from a GCB to a memory B-cell transcriptional signature.
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CEO of Professional Science Editing for Scientists @ prosciediting.com