Evidence map›Paper›PMID 25453218›Full record

ReviewAdvances in biological regulation2015

PLCε mediated sustained signaling pathways.

Stephanie S Dusaban, Joan Heller Brown

Open access · greenAbstract readReview
In one paragraph

Review in Advances in biological regulation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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  5. Review
  6. Soluble cyclase-mediated nuclear cAMP synthesis is sufficient for cell proliferation.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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  8. Review
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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

2 authors at 1 institution in 1 country.

Stephanie S DusabanDepartment of Pharmacology, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA; Biomedical Sciences Graduate Program, University of California, San Diego, La Jolla, CA 92093, USA.
Joan Heller BrownDepartment of Pharmacology, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA. Electronic address: jhbrown@ucsd.edu.
University of California, San Diego · US

Funding

GRADUATE TRAINING IN CELLULAR &MOLECULAR PHARMACOLOGYT32GM007752 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROWN, JOAN HELLER, HANDEL, TRACY M · 1985 to 2023
$13.5M
THROMBIN, GALPHA12, AND RHO AND CELL GROWTHR01GM036927 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROWN, JOAN HELLER · 1986 to 2012
$3.4M
Rho- and GPCR-mediated signaling through novel cellular effectorsR56GM036927 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROWN, JOAN HELLER · 2008 to 2008
$302k
NIGMS NIH HHS GM 36927NIGMS NIH HHS R01 GM036927NIGMS NIH HHS R56 GM036927NIGMS NIH HHS T32 GM007752
6 · The paper itself

Abstract

Phospholipase C-ε (PLCε) integrates signaling from G-protein coupled receptors (GPCRs) to downstream kinases to regulate a broad range of biological and pathophysiological responses. Relative to other PLCs, PLCε is unique in that it not only serves a catalytic function in phosphoinositide hydrolysis but also functions as an exchange factor small the low molecular weight G-protein Rap1. PLCε is selectively stimulated by agonists for GPCRs that couple to RhoA, which bind directly to the enzyme to regulate its activity. Rap1 also regulates PLCε activity by binding to its RA2 domain and this generates a feedback mechanism allowing sustained signaling. As a result of its regulation by inflammatory ligands for GPCRs and its ability to promote chronic signals, PLCε has been implicated in diseases ranging from cancer to ischemia/reperfusion injury. This review will discuss the regulation of PLCε, molecular mechanisms that contribute to sustained signaling, and the role of the enzyme in various disease contexts.

Indexed as

Signal TransductionAnimalsHumansNeoplasm ProteinsNeoplasmsPhosphatidylinositolsPhosphoinositide Phospholipase CProtein Structure, TertiaryReceptors, G-Protein-CoupledReperfusion InjuryrhoA GTP-Binding ProteinShelterin ComplexTelomere-Binding ProteinsNeoplasm ProteinsPhosphatidylinositolsPhosphoinositide Phospholipase Cphospholipase C epsilonReceptors, G-Protein-CoupledrhoA GTP-Binding ProteinRHOA protein, humanShelterin ComplexTelomere-Binding ProteinsTERF2IP protein, humanDiacylglycerol (DAG)GolgiG-protein coupled receptors (GPCRs)Inositol 1,4,5-trisphosphate (IP3)Phosphatidylinositol4,5-bisphosphate (PIP2)Phospholipase C-ε (PLCε)Protein kinase D(PKD)Rap1RasRhoA

Identifiers

PMID25453218
PMCPMC4314097
OpenAlexW2040151256

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.