Activation of @entity1366 by @entity10185 in response to XXXX -induced cell death in @entity1 gingival fibroblasts.

@entity1 @entity274 @entity8047 @entity3963 @entity1441 @entity855 @entity273 @entity866 @entity18942 @entity6164 @entity4286 @entity669 @entity11616 @entity1366 @entity10185
@entity273 ( @entity274 ) increases protein @entity669 phosphorylation of numerous proteins in @entity1 gingival fibroblasts (HGFs). Two main proteins, with an apparent molecular weight of 44 and 42kDa, were phosphorylated after @entity273 stimulation of the @entity1 gingival fibroblasts. Further analysis identified these two proteins as @entity1366 . Maximum phosphorylation was detected at 10min post- @entity274 treatment. Pretreatment with an @entity8047 inhibitor, @entity4286 , inhibited @entity274 -stimulated @entity1366 phosphorylation in a dose-dependent manner. Treatment with @entity274 also induced phosphorylation of @entity10185 ( @entity10185 ). @entity866 , a @entity6164 inhibitor, blocked @entity1366 phosphorylation induced by @entity274 . In addition, @entity274 -induced cell death was prevented by @entity4286 , @entity1441 , and @entity11616 , which are @entity8047 , @entity3963 and @entity6164 inhibitors, respectively. These results suggest that @entity274 leads to the phosphorylation and activation of @entity1366 in a @entity6164 -dependent manner. These findings demonstrate that the MAPK signaling pathway plays an active role in mediating the @entity274 -induced decrease in @entity18942 cell viability and @entity855 depletion.
