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AHSA1 — DUSP1

Text-mined interactions from Literome

Nimah et al., Shock 2005 : Contribution of MKP-1 regulation of p38 to endotoxin tolerance
Zhou et al., Cancer Res 2006 (Breast Neoplasms) : Furthermore, we show by small interfering RNA silencing that down-regulation of MKP-1 increases phosphorylated p38 and JNK and subsequent cell death induced by H ( 2 ) O ( 2 )
Hu et al., Cell Signal 2007 : These results indicate a critical role of p38-MK2 dependent induction of MKP-1 in innate immune responses
Zhou et al., Proc Natl Acad Sci U S A 2008 : MKP-1 inhibits high NaCl induced activation of p38 but does not inhibit the activation of TonEBP/OREBP : opposite roles of p38alpha and p38delta
Wang et al., Life Sci 2008 (Endotoxemia) : Our results indicate that the inhibition of p38 and JNK activities by glucocorticoids is mediated by enhanced Mkp-1 expression
Kar et al., J Leukoc Biol 2010 (Leishmaniasis, Visceral) : Inhibition of these phosphatases prior to infection points toward preferential induction of the Th2 response through deactivation of p38 by MKP1
Li et al., J Cell Biochem 2010 : Interestingly, p38 activation, a common process mediating various biological effects of LPA, was inhibited by LPA in this study, and the regulation of p38 pathway by LPA was dependent on LPA ( 1/3 ) /Gi/ERK1/2 pathway mediated MKP-1 induction but independent of PI3K/Akt pathway
Rastogi et al., Am J Respir Crit Care Med 2011 (Sarcoidosis, Pulmonary) : Our results suggest that enhanced p38 signaling in response to microbial products is caused by abnormal regulation of MKP-1 and contributes to heightened inflammation in sarcoidosis
Ndong et al., Molecular pain 2012 (Disease Models, Animal...) : We observed that in vitro overexpression of MKP-1 blocked lipopolysaccharide induced phosphorylation of p38 ( and other MAPKs ) as well as release of pro-algesic effectors ( i.e., cytokines, chemokines, nitric oxide )
Niisato et al., American journal of physiology. Renal physiology 2012 : Hypotonic stress activates p38 , which in turn induces MKP-1 and to a lesser extent MKP-3 mRNA expression
Auger-Messier et al., Circ Res 2013 (Cardiomyopathies...) : Although single nulls showed no molecular effects, combined disruption of Dusp1/4 promoted unrestrained p38 MAPK activity in both mouse embryonic fibroblasts and the heart, with no change in the phosphorylation of c-Jun N-terminal kinases or extracellular signal regulated kinases at baseline or with stress stimulation