Evidence map›Paper›PMID 29263900›Full record

ArticleSignal transduction and targeted therapy

G-protein-coupled receptors mediate 14-3-3 signal transduction.

Hua Li, Alex Eishingdrelo, Sathapana Kongsamut, Haifeng Eishingdrelo

Abstract read
In one paragraph

Article in Signal transduction and targeted therapy. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Review
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  5. [NKD1 promotes glucose uptake in colon cancer cells by activating YWHAE transcription].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
    Article
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  7. Review
  8. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Hua LiBioInvenu Corp., East Hanover, New Jersey, USA.
Alex EishingdreloBioInvenu Corp., East Hanover, New Jersey, USA.
Sathapana KongsamutRudder Serendip LLC, Madison, New Jersey, USA.
Haifeng EishingdreloBioInvenu Corp., East Hanover, New Jersey, USA.

Funding

Novel tools for investigating GPCR-mediated 14-3-3 signaling pathwayR44MH108203 · NIMH · BIOINVENU CORPORATION · PI EISHINGDRELO, HAIFENG · 2017 to 2018
$1.5M
Novel tools for investigating GPCR-mediated 14-3-3 signaling pathwayR43MH108203 · NIMH · BIOINVENU CORPORATION · PI EISHINGDRELO, HAIFENG · 2016 to 2016
$331k
Novel tools for identifying GPCR compounds modulating specific sub-cellular ERK aR43MH101903 · NIMH · BIOINVENU CORPORATION · PI EISHINGDRELO, HAIFENG · 2013 to 2013
$279k
NIMH NIH HHS R43 MH101903NIMH NIH HHS R43 MH108203NIMH NIH HHS R44 MH108203
6 · The paper itself

Abstract

G-protein-coupled receptor (GPCR)-interacting proteins likely participate in regulating GPCR signaling by eliciting specific signal transduction cascades, inducing cross-talk with other pathways, and fine tuning the signal. However, except for G-proteins and β-arrestins, other GPCR-interacting proteins are poorly characterized. 14-3-3 proteins are signal adaptors, and their participation in GPCR signaling is not well understood or recognized. Here we demonstrate that GPCR-mediated 14-3-3 signaling is ligand-regulated and is likely to be a more general phenomenon than suggested by the previous reports of 14-3-3 involvement with a few GPCRs. For the first time, we can pharmacologically characterize GPCR/14-3-3 signaling. We have shown that GPCR-mediated 14-3-3 signaling is phosphorylation-dependent, and that the GPCR/14-3-3 interaction likely occurs later than receptor desensitization and internalization. GPCR-mediated 14-3-3 signaling can be β-arrestin-independent, and individual agonists can have different potencies on 14-3-3 and β-arrestin signaling. GPCRs can also mediate the interaction between 14-3-3 and Raf-1. Our work opens up a new broad realm of previously unappreciated GPCR signal transduction. Linking GPCRs to 14-3-3 signal transduction creates the potential for the development of new research directions and provides a new signaling pathway for drug discovery.

Identifiers

PMID29263900
PMCPMC5661649

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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 OpenQuestion graph.