Evidence map›Paper›PMID 32840039›Full record

ArticleEMBO reports2020

Keys to the Kingdom: GPCR phosphorylation patterns direct β-arrestin.

Richard T Premont

Open access · greenAbstract readComment
In one paragraph

Article in EMBO reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 43% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 7 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Richard T PremontHarrington Discovery Institute, University Hospitals Cleveland Medical Center, Cleveland, OH, USA.
Case Western Reserve University · US

Funding

Regulation of Beta-Adrenergic Receptor Signaling by S-NitrosylationP01HL075443 · NHLBI · DUKE UNIVERSITY · PI XIAO, KUNHONG · 2004 to 2019
$26.1M
A Molecular Approach to the Pathogenesis of Portal HypertensionR01DK113159 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI DON C. ROCKEY · 2017 to 2026
$2.7M
NHLBI NIH HHS P01 HL075443NIDDK NIH HHS R01 DK113159NIH HHS P01 HL075443NIH HHS R01 DK113159
6 · The paper itself

Abstract

The β-arrestin proteins are key regulators of G protein-coupled receptors, serving at least three distinct functions: inhibiting receptor signaling through G proteins, directing receptor trafficking from the cell surface after activation, and transmitting receptor-initiated signals directly. How the two β-arrestin proteins perform these many functions for hundreds of receptor types throughout the body, and specifically how β-arrestin-mediated signaling can be tuned to cellular conditions, remains an open question. Function-based evidence and recent structure-based evidence have suggested that patterns of receptor phosphorylation ("barcodes") may be a critical determinant of β-arrestin action. In this issue of EMBO Reports, Baidya and colleagues (Baidya et al, 2020a) report that specific receptor phosphorylation site clusters ("codes") determine whether β-arrestin 1 acts to promote or inhibit receptor activation of Erk mitogen-activated protein kinases. They provide direct evidence for a functional barcode system by transferring inhibitory and stimulatory codes between receptors, suggesting future work to understand just how code site location in a receptor and its phosphorylation status can lead to very different functions of bound β-arrestin proteins.

Indexed as

ArrestinsMAP Kinase Signaling Systembeta-Arrestin 1beta-ArrestinsPhosphorylationArrestinsbeta-Arrestin 1beta-Arrestins

Identifiers

PMID32840039
PMCPMC7507377
OpenAlexW3080923570

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.