Asterisk indicates models that included modification by n-terminal acetylation.
Here we show that the increased glycosylation induced by glucose deprivation and detected by CTD110.6 antibodies is actually modification by N-GlcNAc2, rather than by O-GlcNAc.
Unlike human Arl6 which has a ciliary localisation, TbARL6 is associated with electron-dense vesicles throughout the cell body following co-translational modification by N-myristoylation.
Unconditional logistic regression models were used to examine the associations between COX-2 genotypes and risk of colorectal cancer, and their possible modification by n-6 PUFA intake.
The variable modifications allowed were oxidation (methionine), phosphylation (serine/tyrosine/threonine), acetylation (histidine/serine/tyrosine/threonine), modification by N-acetylglucosamine (asparginine/serine/threonine), modification by hexose-linked N-acetylglucosamine (serine/threonine) and iTRAQ™ 8-plex (tyrosine).
However, a recent study has shown that increased glycosylation induced by glucose deprivation is actually modification by N-GlcNAc2, and suggests that repression of mature N-linked glycoproteins due to increased levels of N-GlcNAc2-modified proteins represents a newly recognized pathway for effective use of sugar under stress and deprivation conditions [ 30].
The results suggested that the surface-modified anhydrates were more stable in high humidity condition than intact, and the surface-modification by n-butanol or n-propanol adsorption was more effective than that by ethanol.
Zebrafish β subunits are also likely to exhibit post-translational modification by amide nitrogen (N -linked glycosylatioN -linkedfeature of all 4 mammalian β subunits [ 10- 13].
We designed hierarchical structure by immobilizing Cu nanocluster on the surfaces of Ag seeds loaded electrospun polyacrylonitrile (PAN) nanofibers and followed with a surface modification process by n-hexadecyl mercaptan immersion.
In the present work we describe the synthesis and antiproliferative evaluation of a focused library of 30 novel oxazolidines designed by modification of N-substituent, by ring variation, by alkyl variation or by extension of the structure.
This effect might be mediated by several modifications induced by n-3 PUFAs including COX-2 inhibition, downregulation of the antiapoptotic bcl-2 gene and finally by an antiangiogenic effect.
