Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.7.11.13 (
protein kinase C
)
49,245
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
N-acetylglucosaminyltransferase III
(GnT-III) is a key enzyme that inhibits the extension of N-glycans by introducing a bisecting N-acetylglucosamine residue. Our previous studies have shown that modification of N-glycans by GnT-III affects a number of intracellular signaling pathways. In this study, the effects of GnT-III on the cellular response to reactive oxygen species (ROS) were examined. We found that an overexpression of GnT-III suppresses H(2)O(2)-induced apoptosis in HeLaS3 cells. In the case of GnT-III transfectants, activation of Jun N-terminal kinase (JNK) following H(2)O(2) treatment was markedly reduced compared with control cells. Either the depletion of
protein kinase C
(
PKC
) by prolonged treatment with phorbol 12-myristate 13-acetate or the inhibition of
PKC
by the specific inhibitor H7 attenuated the H(2)O(2)-induced activation of JNK1 and apoptosis in control cells but not in the GnT-III transfectants. Furthermore, we found that H(2)O(2)-induced phosphorylation of
PKC
delta was markedly suppressed in GnT-III transfectants. Rottlerin, a specific inhibitor of
PKC
delta, significantly inhibited H(2)O(2)-induced activation of JNK1 in control cells, indicating that
PKC
delta is involved in the pathway. These findings suggest that the overexpression of GnT-III suppresses H(2)O(2)-induced activation of
PKC
delta-JNK1 pathway, resulting in inhibition of apoptosis.
...
PMID:Down-regulation of hydrogen peroxide-induced PKC delta activation in N-acetylglucosaminyltransferase III-transfected HeLaS3 cells. 1242 58
