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January 9, 2009Circulation ResearchOpen Access

AMP-Activated Protein Kinase Functionally Phosphorylates Endothelial Nitric Oxide Synthase Ser633

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Population

Mouse models (including AMPKalpha2(-/-) mice) and vascular endothelial cells (ECs)

Comparison

AMPK activation via shear stress, atorvastatin… vs Pharmacological inhibition or genetic ablation…

Design

Preclinical

Authors

ZCZhen ChenIPI‐Chen PengWSWei Sun

Discussion

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Overview

May guide endothelial NO research; leaves open human translation from animal models.

Structured PICO

P
Population
Mouse models (including AMPKalpha2(-/-) mice) and vascular endothelial cells (ECs)
I
Intervention
AMPK activation via shear stress, atorvastatin, adiponectin, or AMPK agonists (e.g., AICAR)
C
Comparator
Pharmacological inhibition or genetic ablation of AMPK, or untreated controls
O
Outcome
Phosphorylation of eNOS Ser633 and NO productionsurrogate

AMPK-mediated phosphorylation of eNOS Ser633 is a key signaling event for maintaining NO bioavailability and cardiovascular homeostasis.

Cite This Study

Chen et al. (2009) studied this question.

synapsesocial.com/papers/6a7cb270178e986690cf864fhttps://doi.org/10.1161/circresaha.108.187567
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