Of two large intron 1 deletions that took place during primate evolution, only the Hominini-specific event influenced splicing by enhancing IR, most likely by eliminating a G5-containing enhancer, whereas the largest but splicing-neutral deletion was observed in colobines (Supplemental Figs. 4, 5).
More recently, DNA release from a polymer substrate or scaffold has been shown to enhance gene transfer, likely by increasing DNA concentrations in the cell microenvironment.
Activation and inhibition of mTOR, respectively, repress and enhance autophagy, most likely by controlling the assembly of ATG1 complex during the induction of autophagy [9], [10], [11].
These physicochemical properties help enhance nerve regeneration likely by promoting Schwann cell proliferation, neurite extension, and myelination [ 49– 51].
Surface display has been shown to enhance immune responses, likely by increasing the degree of B-cell receptor cross-linking and subsequent B-cell activation.
At position P2′, introduction of a proline mutation enhances self-cleavage, likely by stabilizing the β-turn around the scissile bond and thereby promoting the cleavage-competent state of LexA.
However, the expression of β-gal activity by SMdC-PnlmAB was highly inconsistent with those of other reports [ 6, 7], suggesting that the expression of nlmAB gene was likely enhanced by an unknown factor following initial activation by CSP.
The presentation of the epitope to P6-specific CD4+ T cells is likely enhanced by the presence of the lipid motif on the antigen when endocytosed by the APC upon recognition by TLR2.
The presence of BI-1 inhibited the transforming growth factor- β1-induced epithelial mesenchymal transition of epithelial pulmonary cells and bleomycin-induced pulmonary fibrosis in a mouse model by enhancing collagen degradation, most likely by enhanced activation of the lysosomal V-ATPase through glycosylation.
Re-population was likely enhanced by higher fecundity, homing instinct, and greater mobility of the larger migratory fish.
