Hypoxia increases Hsp90 binding to eNOS via PI3K-Akt in porcine coronary artery endothelium (Q44683780)

5 December 2017

title

Hypoxia increases Hsp90 binding to eNOS via PI3K-Akt in porcine coronary artery endothelium (English)

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5 December 2017

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Jian-xiong Chen

1

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5 December 2017

Barbara Meyrick

series ordinal

2

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5 December 2017

publication date

1 February 2004

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5 December 2017

published in

Laboratory Investigation

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5 December 2017

volume

84

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5 December 2017

issue

2

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5 December 2017

page(s)

182-190

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https://scigraph.springernature.com/pub.10.1038/labinvest.3700027

5 December 2017

exact match

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cites work

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Chronic hypoxia increases endothelial nitric oxide synthase generation of nitric oxide by increasing heat shock protein 90 association and serine phosphorylation

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Moderate hypoxia increases heat shock protein 90 expression in excised rat aorta

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7 January 2021

Induction of nitric oxide synthase mRNA by shear stress requires intracellular calcium and G-protein signals and is modulated by PI 3 kinase

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7 January 2021

Hypoxia activates nitric oxide synthase and stimulates nitric oxide production in porcine coronary resistance arteriolar endothelial cells

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7 January 2021

Enhanced electron flux and reduced calmodulin dissociation may explain "calcium-independent" eNOS activation by phosphorylation

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7 January 2021

Long-term L-arginine supplementation improves small-vessel coronary endothelial function in humans

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7 January 2021

Chaperone function of Hsp90-associated proteins

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7 January 2021

Bradykinin-regulated interactions of the mitogen-activated protein kinase pathway with the endothelial nitric-oxide synthase

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7 January 2021

Protein kinase B/Akt activates c-Jun NH(2)-terminal kinase by increasing NO production in response to shear stress.

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7 January 2021

10.1038/LABINVEST.3700027

Identifiers

DOI

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5 December 2017

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