Stromal cell–derived factor 2 is critical for Hsp90-dependent eNOS activation
نویسندگان
چکیده
منابع مشابه
p38 MAPK-dependent eNOS upregulation is critical for 17 -estradiol-mediated cardioprotection following trauma-hemorrhage
Kan WH, Hsu JT, Ba ZF, Schwacha MG, Chen JG, Choudhry MA, Bland KI, Chaudry IH. p38 MAPK-dependent eNOS upregulation is critical for 17 -estradiol-mediated cardioprotection following trauma-hemorrhage. Am J Physiol Heart Circ Physiol 294: H2627–H2636, 2008. First published April 11, 2008; doi:10.1152/ajpheart.91444.2007.—Studies have shown that p38 MAPK and nitric oxide (NO), generated by endot...
متن کاملp38 MAPK-dependent eNOS upregulation is critical for 17beta-estradiol-mediated cardioprotection following trauma-hemorrhage.
Studies have shown that p38 MAPK and nitric oxide (NO), generated by endothelial NO synthase (eNOS), play key roles under physiological and pathophysiological conditions. Although administration of 17beta-estradiol (E2) protects cardiovascular injury from trauma-hemorrhage, the mechanism by which E2 produces those effects remains unknown. Our objective was to determine whether the E2-mediated a...
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Endothelial nitric oxide synthase (eNOS), which generates the endogenous vasodilator, nitric oxide (NO), is highly regulated by post-translational modifications and protein interactions. We recently used purified proteins to characterize the mechanisms by which heat shock protein 90 (HSP90) increases eNOS activity at low and high Ca levels (Takahashi, S. and Mendelsohn, M. E., J. Biol. Chem. 27...
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1. The L-arginine-NO pathway has been implicated in the vasorelaxant effect of 17-beta-oestradiol. Here we have addressed the involvement of two distinct activation steps of endothelial nitric oxide synthase (eNOS) in the 17-beta-oestradiol-induced vasorelaxant effect on rat aortic rings. 2. Rat aortic rings contracted with phenylephrine (PE) 1 microM relaxed in a concentration related fashion ...
متن کاملRASA3 is a critical inhibitor of RAP1-dependent platelet activation.
The small GTPase RAP1 is critical for platelet activation and thrombus formation. RAP1 activity in platelets is controlled by the GEF CalDAG-GEFI and an unknown regulator that operates downstream of the adenosine diphosphate (ADP) receptor, P2Y12, a target of antithrombotic therapy. Here, we provide evidence that the GAP, RASA3, inhibits platelet activation and provides a link between P2Y12 and...
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ژورنال
عنوان ژورنال: Science Signaling
سال: 2015
ISSN: 1945-0877,1937-9145
DOI: 10.1126/scisignal.aaa2819