Evidence map›Paper›PMID 28655771›Full record

ArticleThe Journal of biological chemistry2017

p115 RhoGEF activates the Rac1 GTPase signaling cascade in MCP1 chemokine-induced vascular smooth muscle cell migration and proliferation.

Nikhlesh K Singh, Jagadeesh Janjanam, Gadiparthi N Rao

Open access · hybridAbstract readComparative Study
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Monocyte Migration Emerges from a Divergent Chemokine Signaling Network.bioRxiv : the preprint server for biology · 2026
    Article
  3. How Functional Variants Reconfigure the Rac2 Conformational Landscape.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
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  9. Article
  10. Challenges and strategies forBioactive materials · 2021
    Review
  11. Article
  12. Article
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  17. Article
  18. Article
  19. Article
  20. Inflammation in Vein Graft Disease.Frontiers in cardiovascular medicine · 2018
    Review
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

3 authors at 1 institution in 1 country.

Nikhlesh K SinghFrom the Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee 38163. Electronic address: nsingh2@uthsc.edu.
Jagadeesh JanjanamFrom the Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee 38163.
Gadiparthi N RaoFrom the Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee 38163. Electronic address: rgadipar@uthsc.edu.
University of Tennessee Health Science Center · US

Funding

NFATs AND VASCULAR INJURYR01HL069908 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI RAO, GADIPARTHI N · 2002 to 2019
$5.9M
PLA2, EICOSANOIDS AND VASCULAR REMODELINGR01HL064165 · NHLBI · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI RAO, GADIPARTHI N · 2000 to 2016
$5.4M
NHLBI NIH HHS R01 HL064165NHLBI NIH HHS R01 HL069908
6 · The paper itself

Abstract

Although the involvement of Rho proteins in the pathogenesis of vascular diseases is well studied, little is known about the role of their upstream regulators, the Rho guanine nucleotide exchange factors (RhoGEFs). Here, we sought to identify the RhoGEFs involved in monocyte chemotactic protein 1 (MCP1)-induced vascular wall remodeling. We found that, among the RhoGEFs tested, MCP1 induced tyrosine phosphorylation of p115 RhoGEF but not of PDZ RhoGEF or leukemia-associated RhoGEF in human aortic smooth muscle cells (HASMCs). Moreover, p115 RhoGEF inhibition suppressed MCP1-induced HASMC migration and proliferation. Consistent with these observations, balloon injury (BI) induced p115 RhoGEF tyrosine phosphorylation in rat common carotid arteries, and siRNA-mediated down-regulation of its levels substantially attenuated BI-induced smooth muscle cell migration and proliferation, resulting in reduced neointima formation. Furthermore, depletion of p115 RhoGEF levels also abrogated MCP1- or BI-induced Rac1-NFATc1-cyclin D1-CDK6-PKN1-CDK4-PAK1 signaling, which, as we reported previously, is involved in vascular wall remodeling. Our findings also show that protein kinase N1 (PKN1) downstream of Rac1-cyclin D1/CDK6 and upstream of CDK4-PAK1 in the p115 RhoGEF-Rac1-NFATc1-cyclin D1-CDK6-PKN1-CDK4-PAK1 signaling axis is involved in the modulation of vascular wall remodeling. Of note, we also observed that CCR2-G

Indexed as

Models, BiologicalProtein Processing, Post-TranslationalSignal TransductionAnimalsAortaCarotid Artery, CommonCarotid Artery InjuriesCell MovementCell ProliferationCells, CulturedChemokine CCL2Enzyme ActivationHumansMuscle, Smooth, VascularNeointimaPhosphorylationARHGEF1 protein, humanCCL2 protein, humanChemokine CCL2rac1 GTP-Binding ProteinRAC1 protein, humanRho Guanine Nucleotide Exchange Factorscell migrationcell proliferationguanine nucleotide exchange factor (GEF)NFAT transcription factorvascular smooth muscle cells

Identifiers

PMID28655771
PMCPMC5572933
OpenAlexW2731370178

What OpenQuestion holds

Textmetadata
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.