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Histone modifications, such as methylation and acetylation, or incorporation of histone variants can alter nucleosomal dynamics.
An illness, physical exercise, a delay in snack time as well as a host of other variants can alter blood sugar levels, which is why frequent monitoring is critical.
NTSR1 gene variants can alter neurotensin function in the central nervous system, which in turn modulates the DA system serving WM functions [41].
Variants can alter transcription factor binding affinity, subsequently affecting transcription levels of target genes [ 1].
These variants can alter the amino acid transcript or the length of the ORF and directly impact the structure of the protein.
It is well established that genetic variants can alter mRNA folding [ Shen et al., 1999], which in turn can influence function [ Halvorsen et al., 2010].
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Genetic variation can alter transcriptional regulatory activity contributing to variation in complex traits and risk of disease, but identifying individual variants that affect regulatory activity has been challenging.
Mapping of genetic variations, such as single-nucleotide polymorphisms (SNPs), in the human genome has given rise to the idea that combinations of variant genes can alter susceptibility to various diseases.
These are known as fusion proteins, promising variants of which can alter gene expression or, in the case of a technology known as base-editing, alter one base or nucleotide in the DNA with pinpoint accuracy.
However, whether the genetic variants in TLR3 can alter susceptibility to NPC by affecting the anti-EBV immune responses is unknown.
Substitutions of histone variants can change multiple histone DNA and histone histone contacts simultaneously and are well-known for altering characteristics of single nucleosomes and chromatin fibers.
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