Evidence map›Paper›PMID 34111428›Full record

ReviewThe American journal of pathology2021

The Role of R-Ras Proteins in Normal and Pathologic Migration and Morphologic Change.

Shannon M Weber, Steven L Carroll

Open access · greenAbstract readReview
In one paragraph

Review in The American journal of pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  4. RRAS and RRAS2 Mutations Are Recurrent Oncogenic Drivers in Lung Cancer and Are Sensitive to the Pan-RAS Inhibitor RMC-6236.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
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  8. Review
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  15. M-Ras distinct activation scenarios: A mechanistic outlook and targeting.Computational and structural biotechnology journal · 2025
    Article
  16. Review
  17. Article
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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.

Shannon M WeberDepartment of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, South Carolina.
Steven L CarrollDepartment of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, South Carolina. Electronic address: carrolst@musc.edu.
Medical University of South Carolina · US

Funding

South Carolina Cancer Disparities Research Center (SC CaDRe)U54CA210963 · NCI · SOUTH CAROLINA STATE UNIVERSITY · PI WARSHAMANA-GREENE, GNANA SAKUNTALA · 2017 to 2023
$6.1M
Therapeutic Targeting of Receptor Tyrosine Kinase Hierarchies in Schwann Cell Neoplasms - Supplement for DiversityR01NS109655 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI CARROLL, STEVEN L. · 2020 to 2024
$2.1M
Novel Treatment of NF-1 Associated Malignant Peripheral Nerve Sheath TumorsR01CA122804 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CARROLL, STEVEN L. · 2008 to 2012
$1.5M
Role of Neuregulin-1 in Schwann Cell NeoplasiaR01NS048353 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CARROLL, STEVEN L. · 2004 to 2008
$1.3M
The Role of HER3 and IGF1R, through Non-Classical Ras Signaling, on Malignant Peripheral Nerve Sheath Tumor ProgressionF30CA247139 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI DOUTT, SHANNON WEBER · 2020 to 2023
$180k
NCI NIH HHS F30 CA247139NCI NIH HHS R01 CA122804NCI NIH HHS U54 CA210963NINDS NIH HHS R01 NS048353NINDS NIH HHS R01 NS109655
6 · The paper itself

Abstract

The contributions that the R-Ras subfamily [R-Ras, R-Ras2/teratocarcinoma 21 (TC21), and M-Ras] of small GTP-binding proteins make to normal and aberrant cellular functions have historically been poorly understood. However, this has begun to change with the realization that all three R-Ras subfamily members are occasionally mutated in Noonan syndrome (NS), a RASopathy characterized by the development of hematopoietic neoplasms and abnormalities affecting the immune, cardiovascular, and nervous systems. Consistent with the abnormalities seen in NS, a host of new studies have implicated R-Ras proteins in physiological and pathologic changes in cellular morphology, adhesion, and migration in the cardiovascular, immune, and nervous systems. These changes include regulating the migration and homing of mature and immature immune cells, vascular stabilization, clotting, and axonal and dendritic outgrowth during nervous system development. Dysregulated R-Ras signaling has also been linked to the pathogenesis of cardiovascular disease, intellectual disabilities, and human cancers. This review discusses the structure and regulation of R-Ras proteins and our current understanding of the signaling pathways that they regulate. It explores the phenotype of NS patients and their implications for the R-Ras subfamily functions. Next, it covers recent discoveries regarding physiological and pathologic R-Ras functions in key organ systems. Finally, it discusses how R-Ras signaling is dysregulated in cancers and mechanisms by which this may promote neoplasia.

Indexed as

AnimalsCell MovementHumansNoonan Syndromeras ProteinsSignal Transductionras ProteinsRRAS protein, human

Identifiers

PMID34111428
PMCPMC8420862
OpenAlexW3173121445

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.