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Text-mined interactions from Literome

Arbabi et al., J Surg Res 2001 (Carcinoma...) : Hyperosmolarity induced both p38 and ERK activation within 30 min ; however, only p38 inhibition attenuated osmotic induced COX-2 expression ; inhibition of ERK activation had no effect
Lee et al., Circulation 2004 : Simvastatin activated p38 and Akt in VSMCs, and the respective inhibitors of p38 and phosphoinositide 3-kinase (PI3K) greatly reduced the level of simvastatin induced HO-1, which suggests the involvement of p38 and the PI3K-Akt pathway in HO-1 induction
An et al., Chin Med J (Engl) 2005 (Melanoma) : The expression of phosphorylated JNK and p38 also increased after the treatment with NCTD, and inhibitors of c-Jun NH2-terminal kinase (JNK) and p38 ( SP600125 and SB203580, respectively ) had significant inhibitory effects on the upregulation of phosphorylated JNK and p38 expression
Ahmed et al., J Nutr 2005 : IL-1beta induced phosphorylation of p38-MAPK , but not that of c-Jun-N-terminal kinase or extracellular regulated kinase, was most susceptible to inhibition by low doses of PFE, and the addition of PFE blocked the activity of p38-MAPK in a kinase activity assay
Qi et al., J Biol Chem 2007 (Breast Neoplasms) : In cells expressing both proteins, p38alpha phosphorylation decreases p38gamma protein expression, whereas its inhibition increases cellular p38gamma concentrations, indicating an active role of p38alpha phosphorylation in negatively regulating p38gamma protein expression
Wu et al., Free Radic Biol Med 2009 (MAP Kinase Signaling System) : Activation of JNK and p38MAPK was weaker in TNFalpha plus PY-treated NOS2 ( -/- ) mice and 1400W and NAC blocked the activation of JNK and p38MAPK in wild-type mice
Sheng et al., J Neuroimmune Pharmacol 2009 (MAP Kinase Signaling System) : IL-1beta triggered the activation of p38 and ERK1/2 ( p44/42) MAP kinase (MAPK) signaling pathways, but WIN55,212-2 mainly inhibited p38 MAPK phosphorylation
Huang et al., J Cell Physiol 2010 (MAP Kinase Signaling System) : The expressions of either p38alpha ( AF ) or p38beta ( AF ) reduced activin A-induced p38 activation, Hb synthesis, and zeta-globin promoter activity
Suwanabol et al., Am J Physiol Heart Circ Physiol 2012 (Carotid Artery Injuries) : Overexpression of Smad3 enhanced p38 phosphorylation and inhibition of p38 with a chemical inhibitor or a small interfering RNA blocked TGF-ß induced Akt phosphorylation
Larsen et al., J Biol Chem 1998 : We conclude that ERK1/2 and p38 activation is necessary but not sufficient for IL-1beta mediated beta-cell NO synthesis and that p38 is involved in signaling of NO-independent effects of IL-1beta in beta-cells