February 16, 2001Circulation ResearchOpen Access

AKAP-Mediated Targeting of Protein Kinase A Regulates Contractility in Cardiac Myocytes

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Population

Cardiac myocytes

Comparison

Adenovirus-mediated gene transfer of Ht31 vs Ht31P and uninfected cells

Design

Preclinical

Authors

MFMary Alexander FinkNational Institutes of Health DZDaniel R. ZakharyWinthrop-University Hospital JMJulie A. MackeyUniversity of Connecticut

Discussion

Member takes

Implication

Enhances beta-adrenergic myocyte contractility despite reduced phosphorylation; extends PKA compartmentalization concepts but leaves open human translation.

Structured PICO

Population

Cardiac myocytes

Intervention

Adenovirus-mediated gene transfer of Ht31 (a peptide that binds PKA regulatory subunit type II with high affinity to disrupt AKAP-mediated PKA anchoring)

Comparator

Ht31P (a proline-substituted derivative that does not bind RII) and uninfected cells

Outcome

RII distribution, Ca(2+) cycling, cell shortening, and PKA-dependent substrate phosphorylationsurrogate

AKAP-mediated targeting of PKA is essential for regulating cardiomyocyte contractile function and substrate phosphorylation in response to beta-adrenergic stimulation.

Cite This Study

Fink et al. (2001) studied this question.

synapsesocial.com/papers/6a817dad17c102c67164abbe https://doi.org/10.1161/01.res.88.3.291

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Implication

Enhances beta-adrenergic myocyte contractility despite reduced phosphorylation; extends PKA compartmentalization concepts but leaves open human translation.

AKAP-Mediated Targeting of Protein Kinase A Regulates Contractility in Cardiac Myocytes

Discussion

Member takes

Implication

Structured PICO

Cite This Study

AKAP-Mediated Targeting of Protein Kinase A Regulates Contractility in Cardiac Myocytes

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider