Evidence map›Paper›PMID 29621614›Full record

ReviewSeminars in cancer biology2019

Ras and Rap1: A tale of two GTPases.

Seema Shah, Ethan J Brock, Kyungmin Ji, Raymond R Mattingly

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

139 citing papers in PubMed, 217 citations in OpenAlex.

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  15. The effect and mechanism of total alkaloids ofFrontiers in pharmacology · 2026
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79 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Seema ShahProgram in Cancer Biology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Ethan J BrockProgram in Cancer Biology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Kyungmin JiDepartment of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Raymond R MattinglyProgram in Cancer Biology, Wayne State University School of Medicine, Detroit, MI 48201, USA; Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI 48201, USA. Electronic address: r.mattingly@wayne.edu.
Wayne State University · US

Funding

"Research Supplement to Promote Diversity in Health-Related Research", as part of Moffitt PS-OC, "Cancer as a Complex adaptive System"U54CA193489 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI ANDERSON, ALEXANDER ROBERTSON ALLAN, GATENBY, ROBERT A · 2015 to 2020
$12.5M
TRAINING PROGRAM IN THE BIOLOGY OF CANCERT32CA009531 · NCI · WAYNE STATE UNIVERSITY · PI Larry H Matherly · 1985 to 2026
$5.3M
Proteolytic Pathways in Progression of Pre-Malignant Breast DiseaseR01CA131990 · NCI · WAYNE STATE UNIVERSITY · PI MATTINGLY, RAYMOND R, SLOANE, BONNIE F · 2008 to 2013
$1.9M
4D Microfluidic Platforms for Targeting Breast Cancer:Lymphatic InteractionsR21CA175931 · NCI · WAYNE STATE UNIVERSITY · PI SLOANE, BONNIE F · 2013 to 2014
$359k
Sprouty4 is a negative regulator of ERK/MAPK signaling in breast cancer and plays a role in the transition from in situ to invasive diseaseF31CA213807 · NCI · WAYNE STATE UNIVERSITY · PI BROCK, ETHAN J · 2017 to 2019
$123k
NCI NIH HHS F31 CA213807NCI NIH HHS R01 CA131990NCI NIH HHS R21 CA175931NCI NIH HHS T32 CA009531NCI NIH HHS U54 CA193489
6 · The paper itself

Abstract

Ras oncoproteins play pivotal roles in both the development and maintenance of many tumor types. Unfortunately, these proteins are difficult to directly target using traditional pharmacological strategies, in part due to their lack of obvious binding pockets or allosteric sites. This obstacle has driven a considerable amount of research into pursuing alternative ways to effectively inhibit Ras, examples of which include inducing mislocalization to prevent Ras maturation and inactivating downstream proteins in Ras-driven signaling pathways. Ras proteins are archetypes of a superfamily of small GTPases that play specific roles in the regulation of many cellular processes, including vesicle trafficking, nuclear transport, cytoskeletal rearrangement, and cell cycle progression. Several other superfamily members have also been linked to the control of normal and cancer cell growth and survival. For example, Rap1 has high sequence similarity to Ras, has overlapping binding partners, and has been demonstrated to both oppose and mimic Ras-driven cancer phenotypes. Rap1 plays an important role in cell adhesion and integrin function in a variety of cell types. Mechanistically, Ras and Rap1 cooperate to initiate and sustain ERK signaling, which is activated in many malignancies and is the target of successful therapeutics. Here we review the role activated Rap1 in ERK signaling and other downstream pathways to promote invasion and cell migration and metastasis in various cancer types.

Indexed as

AnimalsBiomarkers, TumorCell AdhesionEnergy MetabolismEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansIntegrinsMolecular Targeted TherapyMutationNeoplasmsrap1 GTP-Binding Proteinsras ProteinsSignal TransductionBiomarkers, TumorIntegrinsrap1 GTP-Binding Proteinsras ProteinsCell-adhesionEMTERK/MAPKFTIIntegrinsMetabolismRap1Rap1GapRas

Identifiers

PMID29621614
PMCPMC6170734
OpenAlexW2796336382

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.