Evidence map›Paper›PMID 31707029›Full record

ArticleThe Journal of investigative dermatology2020

Activation of G-Protein Coupled Receptor-Gαi Signaling Increases Keratinocyte Proliferation and Reduces Differentiation, Leading to Epidermal Hyperplasia.

M Pilar Pedro, Natalia Salinas Parra, J Silvio Gutkind, Ramiro Iglesias-Bartolome

Open access · greenAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.1field-weighted citation impact, top 51% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Chemogenetic Activation of GFASEB bioAdvances · 2026
    Article
  2. Article
  3. Deletion of p63 exon 13 in mice reveals C-terminal isoform-specific functions in epithelial development.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Keratinocyte-TRPV1 sensory neuron interactions in a genetically controllable mouse model of chronic neuropathic itch.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. YAP/TAZ Signalling Controls Epidermal Keratinocyte Fate.International journal of molecular sciences · 2024
    Review
  6. Article
  7. 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 2 institutions in 1 country.

M Pilar PedroLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
Natalia Salinas ParraLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
J Silvio GutkindMoores Cancer Center, University of California, San Diego, La Jolla, California.
Ramiro Iglesias-BartolomeLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Electronic address: ramiro.iglesias-bartolome@nih.gov.
National Institutes of Health · USUniversity of California San Diego · US

Funding

Signaling pathways regulating stem cell fate decisionsZIABC011763 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI IGLESIAS-BARTOLOME, RAMIRO · 2017 to 2025
$7.5M
G-protein-coupled receptor signaling in cancer development and treatmentZIABC011764 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI IGLESIAS-BARTOLOME, RAMIRO · 2017 to 2022
$1.9M
Intramural NIH HHS ZIA BC011763Intramural NIH HHS ZIA BC011764
6 · The paper itself

Abstract

G-protein coupled receptors (GPCRs) and their associated heterotrimeric G proteins impinge on pathways that control epithelial cell self-renewal and differentiation. Although it is known that Gαs protein signaling regulates skin homeostasis in vivo, the role of GPCR-coupled Gαi proteins in the skin is unclear. Here, by using a chemogenetic approach, we demonstrate that GPCR-Gαi activation can regulate keratinocyte proliferation and differentiation and that overactivation of Gαi-signaling in the basal compartment of the mouse skin can lead to epidermal hyperplasia. Our results expand our understanding of the role of GPCR-cAMP signaling in skin homeostasis and reveal overlapping and divergent roles of the cAMP-regulating heterotrimeric Gαs and Gαi proteins in keratinocytes.

Indexed as

AnimalsCell DifferentiationCell ProliferationEpidermisFemaleGTP-Binding Protein alpha Subunits, Gi-GoHumansHyperplasiaKeratinocytesMaleMiceNIH 3T3 CellsSignal TransductionGTP-Binding Protein alpha Subunits, Gi-Go

Identifiers

PMID31707029
PMCPMC7202966
OpenAlexW2983512074

What OpenQuestion holds

Textmetadata
LicenceTDM
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.