Evidence map›Paper›PMID 32570982›Full record

ArticleInternational journal of molecular sciences2020

Synphilin-1 Interacts with AMPK and Increases AMPK Phosphorylation.

Tianxia Li, Jingnan Liu, Gongbo Guo, Bo Ning, Xueping Li, Guangjing Zhu, Dejun Yang, Timothy H Moran, Wanli W Smith

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Tianxia LiDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Jingnan LiuDepartment of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, MD 21201, USA.ORCID 0000-0002-4325-1796
Gongbo GuoDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Bo NingDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Xueping LiDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Guangjing ZhuDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Dejun YangDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0001-5118-0652
Timothy H MoranDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Wanli W SmithDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.ORCID 0000-0002-6482-5154
Johns Hopkins University · USUniversity of Maryland, Baltimore · US

Funding

Synphilin-1 and ObesityR01DK083410 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI SMITH, WANLI W · 2010 to 2014
$1.7M
NIDDK NIH HHS R01 DK083410NIH HHS DK083410
6 · The paper itself

Abstract

A role for the cytoplasmic protein synphilin-1 in regulating energy balance has been demonstrated recently. Expression of synphilin-1 increases ATP levels in cultured cells. However, the mechanism by which synphilin-1 alters cellular energy status is unknown. Here, we used cell models and biochemical approaches to investigate the cellular functions of synphilin-1 on the AMP-activated protein kinase (AMPK) signaling pathway, which may affect energy balance. Overexpression of synphilin-1 increased AMPK phosphorylation (activation). Moreover, synphilin-1 interacted with AMPK by co-immunoprecipitation and GST (glutathione S-transferase) pull-down assays. Knockdown of synphilin-1 reduced AMPK phosphorylation. Overexpression of synphilin-1 also altered AMPK downstream signaling, i.e., a decrease in acetyl CoA carboxylase (ACC) phosphorylation, and an increase in p70S6K phosphorylation. Treatment of compound C (an AMPK inhibitor) reduced synphilin-1 binding with AMPK. In addition, compound C diminished synphilin-1-induced AMPK phosphorylation, and the increase in cellular ATP (adenosine triphosphate) levels. Our results demonstrated that synphilin-1 couples with AMPK, and they exert mutual effects on each other to regulate cellular energy status. These findings not only identify novel cellular actions of synphilin-1, but also provide new insights into the roles of synphilin-1 in regulating energy currency, ATP.

Indexed as

Acetyl-CoA CarboxylaseAdenosine TriphosphateAMP-Activated Protein KinasesCarrier ProteinsHEK293 CellsHumansNerve Tissue ProteinsPhosphorylationProtein BindingPyrazolesPyrimidinesSignal TransductionACACA protein, humanAcetyl-CoA CarboxylaseAdenosine TriphosphateAMP-Activated Protein KinasesCarrier ProteinsdorsomorphinNerve Tissue ProteinsPyrazolesPyrimidinesSNCAIP protein, humanAMPKATPenergy balanceprotein interactionsynphilin-1

Identifiers

PMID32570982
PMCPMC7352261
OpenAlexW3036337645

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.