Evidence map›Paper›PMID 32350291›Full record

ArticleScientific reports2020

RNA-seq analysis reveals TRPC genes to impact an unexpected number of metabolic and regulatory pathways.

Karina Formoso, Sebastian Susperreguy, Marc Freichel, Lutz Birnbaumer

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 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
0.9field-weighted citation impact, top 24% 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, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. TRP Channels in Stroke.Neuroscience bulletin · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. How TRPC Channels Modulate Hippocampal Function.International journal of molecular sciences · 2020
    Review
  11. Article
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 at 4 institutions in 3 countries.

Karina FormosoInstitute for Biomedical Research (BIOMED UCA-CONICET). School of Medical Sciences, Catholic University of Argentina (UCA), Buenos Aires, C1107AFF, Argentina.
Sebastian SusperreguyInstitute for Biomedical Research (BIOMED UCA-CONICET). School of Medical Sciences, Catholic University of Argentina (UCA), Buenos Aires, C1107AFF, Argentina.
Marc FreichelInstitute of Physiology and Pathophysiology, Heidelberg University, 69120, Heidelberg, Germany.
Lutz BirnbaumerInstitute for Biomedical Research (BIOMED UCA-CONICET). School of Medical Sciences, Catholic University of Argentina (UCA), Buenos Aires, C1107AFF, Argentina. birnbau1@gmail.com.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARHeidelberg University · DENational Institute of Environmental Health Sciences · USPontificia Universidad Católica Argentina · AR

Funding

Transmembrane Signaling Mechanisms Involving TRP ChannelsZ01ES101684 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BIRNBAUMER, LUTZ · 2003 to 2008
$2.1M
Intramural NIH HHS Z01 ES101684
6 · The paper itself

Abstract

The seven-member transient receptor potential canonical genes (TRPC1-7) encode cation channels linked to several human diseases. There is little understanding of the participation of each TRPC in each pathology, considering functional redundancy. Also, most of the inhibitors available are not specific. Thus, we developed mice that lack all of the TRPCs and performed a transcriptome analysis in eight tissues. The aim of this research was to address the impact of the absence of all TRPC channels on gene expression. We obtained a total of 4305 differentially expressed genes (DEGs) in at least one tissue where spleen showed the highest number of DEGs (1371). Just 21 genes were modified in all the tissues. Performing a pathway enrichment analysis, we found that many important signaling pathways were modified in more than one tissue, including PI3K (phosphatidylinositol 3-kinase/protein kinase-B) signaling pathway, cytokine-cytokine receptor interaction, extracellular matrix (ECM)-receptor interaction and circadian rhythms. We describe for the first time the changes at the transcriptome level due to the lack of all TRPC proteins in a mouse model and provide a starting point to understand the function of TRPC channels and their possible roles in pathologies.

Indexed as

RNA-SeqTRPC Cation ChannelsAnimalsGene Expression RegulationGene Regulatory NetworksMetabolic Networks and PathwaysMiceMice, KnockoutSignal TransductionTRPC Cation Channels

Identifiers

PMID32350291
PMCPMC7190874
OpenAlexW3022738561

What OpenQuestion holds

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LicenceCC BY
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 OpenQuestion graph.