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CEP19 — MAPK14

Text-mined interactions from Literome

Hashimoto et al., Am J Respir Crit Care Med 2001 : The results showed that : ( 1 ) TGF-beta1 caused the phenotypic modulation of HLF to myofibroblasts in a dose- and a time dependent manner ; ( 2 ) TGF-beta1 induced increases in c-Jun-NH2- terminal kinase (JNK), p38 MAPK, and extracellular signal regulated kinase ( Erk ) phosphorylation and activity ; ( 3 ) the inhibitors CEP-1347, SB 203580, and PD 98059 attenuated TGF-beta1 induced JNK, p38 MAPK , and Erk activity, respectively ; and ( 4 ) CEP-1347 , but not SB 203580 or PD 98059, attenuated the TGF-beta1 induced phenotypic modulation of HLF to myofibroblasts in a dose dependent manner
Furuichi et al., Respirology 2002 (Asthma, Exercise-Induced...) : The results showed that : ( i ) hyperosmolarity induced the threonine and tyrosine phosphorylation of p38 MAPK and JNK ; ( ii ) SB 203580, as the specific inhibitor of p38 MAPK activity, and CEP 11004 attenuated hyperosmolarity induced p38 MAPK and JNK activity, respectively ; ( iii ) SB 203580 and CEP 11004, but not PD 98059, partially attenuated IL-8 and RANTES production ; and ( iv ) a combination of SB 203580 and CEP 11004 attenuated IL-8 and RANTES production in an additive fashion
Hayashi et al., Respirology 2008 (Influenza, Human) : The expression of 29 genes was inhibited either by SB 203580, a specific inhibitor of p38 MAPK , or by CEP-11004 , a specific inhibitor of the c-Jun-N-terminal kinase (JNK) cascade, and the percentage inhibition by SB 203580 correlated with that by CEP-11004, suggesting that p38 and JNK participate in a common downstream pathway involved in the regulation of gene expression