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These findings suggest that both histone modifications and extracellular histones contribute to central nervous system disease.
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These results suggest a propensity for miR-29b to target genes associated with DNA modification and extracellular matrix (ECM) activities (Fig. 5, Additional file 6: Table S3), in contrast to miR-223 whose putative targets appeared to fall into nucleoside catabolic processes (particularly purine metabolism) and GTPase regulators (Fig. 6, Additional file 7: Table S4).
The categories of "Nuclear structure" (90, 0.35%), "Secondary metabolites biosynthesis, transport and catabolism"(519, 2.0%), "RNA processing and modification" (1,121,4.4%), and "Extracellular structures" (62, 0.24%) had the least proportions.
It depends on target complementarity, 3′-end modification, cellular condition, and extracellular signaling (Katoh et al. 2009; Rüegger and Großhans 2012).
Glycosylation is the most common post-translational modification of TMPs and extracellular proteins, in which the side chain of Asp (N-Glycosylation) or of Ser/Thr/Trp (O-Glycosylation) is modified by the attachment of a sugar component.
These MMP activities are required for the proteolytic modifications of basements membranes and extracellular matrices during angiogenesis.
The cellular microenvironment and modifications of extracellular matrix components (ECM) are closely correlated to malignant transformation and all the steps of the metastatic cascade [ 110, 111].
In fact, they are distributed in nearly all subclasses of three larger classes, except for RNA processing and modification, nuclear structure, cytoskeleton and extracellular structures (data not shown).
Glycosylation is an essential form of post-translational modification that regulates intracellular and extracellular processes.
This protein family is an important role player for many biological functions such as cell migration, proliferation, differentiation, and extracellular modification [ 96].
Hudecek, M. et al. Receptor affinity and extracellular domain modifications affect tumor recognition by ROR1-specific chimeric antigen receptor T cells.
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