| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-81 |
Sentence |
denotes |
Targeting O-glycosyltransferase (OGT) to promote healing of diabetic skin wounds. |
| T2 |
82-139 |
Sentence |
denotes |
Non-healing wounds are a significant source of morbidity. |
| T3 |
140-229 |
Sentence |
denotes |
This is particularly true for diabetic patients, who tend to develop chronic skin wounds. |
| T4 |
230-487 |
Sentence |
denotes |
O-GlcNAc modification of serine and threonine residues is a common regulatory post-translational modification analogous to protein phosphorylation; increased intracellular protein O-GlcNAc modification has been observed in diabetic and hyperglycemic states. |
| T5 |
488-765 |
Sentence |
denotes |
Two intracellular enzymes, UDP-N-acetylglucosamine-polypeptide β-N-acetylglucosaminyl transferase (OGT) and O-GlcNAc-selective N-acetyl-β-D-glucosaminidase (OGA), mediate addition and removal, respectively, of N-acetylglucosamine (GlcNAc) from intracellular protein substrates. |
| T6 |
766-1049 |
Sentence |
denotes |
Alterations in O-GlcNAc modification of intracellular proteins is linked to diabetes, and the increased levels of protein O-GlcNAc modification observed in diabetic tissues may in part explain some of the observed underlying pathophysiology that contributes to delayed wound healing. |
| T7 |
1050-1250 |
Sentence |
denotes |
We have previously shown that increasing protein O-GlcNAc modification by overexpression of OGT in murine keratinocytes results in elevated protein O-GlcNAc modification and a hyperadhesive phenotype. |
| T8 |
1251-1471 |
Sentence |
denotes |
This study was undertaken to explore the hypothesis that increased O-GlcNAc modification of cellular proteins in diabetic skin could contribute to the delayed wound healing observed in patients with diabetic skin ulcers. |
| T9 |
1472-1674 |
Sentence |
denotes |
In the present study, we show that human keratinocytes cultured under hyperglycemic conditions display increased levels of O-GlcNAc modification as well as a delay in the rate of wound closure in vitro. |
| T10 |
1675-1879 |
Sentence |
denotes |
We further show that specific knockdown of OGT by RNA interference (RNAi) reverses this effect, thereby opening up the opportunity for OGT-targeted therapies to promote wound healing in diabetic patients. |
