What is the clinical evidence from this study?

Study design: Other. Intervention: beta-arrestin. Primary outcome: signaling function of beta ARK-phosphorylated beta-adrenergic receptors.

What question did this study set out to answer?

To identify and clone the cofactor required for beta-adrenergic receptor kinase (beta-ARK) to mediate homologous desensitization of beta-adrenergic receptors.

June 22, 1990Science

β-Arrestin: a Protein that Regulates β-adrenergic Receptor Function

Q: What does this research mean for the field?

Beta-arrestin acts as a necessary cofactor that inhibits the signaling function of beta ARK-phosphorylated beta-adrenergic receptors by more than 75 percent. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

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Key result

Beta-arrestin inhibited the signaling function of beta ARK-phosphorylated beta-adrenergic receptors by more than 75 percent.

Population

In vitro molecular model studying beta-adrenergic receptors and beta-arrestin

Design

Preclinical

Authors

MLMartin J. LohseHeart Failure & Transplant JBJeffrey BenovicThomas Jefferson University JCJuan CodinaElectrophysiology

Discussion

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Implication

Highlights beta-arrestin’s role in receptor regulation; extends beta ARK findings but leaves open therapeutic implications.

Key Points

To identify and clone the cofactor required for beta-adrenergic receptor kinase (beta-ARK) to mediate homologous desensitization of beta-adrenergic receptors.
Cloned complementary DNA encoding the cofactor homologous to visual arrestin.
Expressed and partially purified the 418-amino acid protein designated beta-arrestin.
Assayed signaling inhibition on beta-ARK-phosphorylated beta-adrenergic receptors and rhodopsin.
Cloned cDNA encoding a 418-amino acid protein with structural homology to retinal arrestin.
Partially purified beta-arrestin inhibited signaling of beta-ARK-phosphorylated beta-adrenergic receptors by >75%, while showing no inhibitory effect on rhodopsin.

Structured PICO

Population

In vitro molecular model studying beta-adrenergic receptors and beta-arrestin

Intervention

Expression and partial purification of beta-arrestin

Outcome

Inhibition of signaling function of beta ARK-phosphorylated beta-adrenergic receptorssurrogate

The discovery and cloning of beta-arrestin reveals its critical role as a cofactor with beta ARK in the homologous desensitization of beta-adrenergic receptors.

Cite This Study

Lohse et al. (1990) studied this question. beta-arrestin was evaluated on signaling function of beta ARK-phosphorylated beta-adrenergic receptors. Beta-arrestin inhibited the signaling function of beta ARK-phosphorylated beta-adrenergic receptors by more than 75 percent.

synapsesocial.com/papers/6a15fa2fbdb7c25666524c99 https://doi.org/10.1126/science.2163110

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β-Arrestin: a Protein that Regulates β-adrenergic Receptor Function

Discussion

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Implication

Key Points

Structured PICO

Cite This Study

β-Arrestin: a Protein that Regulates β-adrenergic Receptor Function

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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