Evidence map›Paper›PMID 29330521›Full record

ArticleScientific reports2018

RGS7 is recurrently mutated in melanoma and promotes migration and invasion of human cancer cells.

Nouar Qutob, Ikuo Masuho, Michal Alon, Rafi Emmanuel, Isadora Cohen, Antonella Di Pizio, Jason Madore, Abdel Elkahloun, Tamar Ziv, Ronen Levy and 14 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  5. Review
  6. A RGS7-CaMKII complex drives myocyte-intrinsic and myocyte-extrinsic mechanisms of chemotherapy-induced cardiotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

24 authors at 7 institutions in 3 countries.

Nouar QutobMolecular Cell Biology Department, Weizmann Institute of Science, Rehovot, Israel.
Ikuo MasuhoDepartment of Neuroscience, The Scripps Research Institute, FL, 33458, USA.
Michal AlonMolecular Cell Biology Department, Weizmann Institute of Science, Rehovot, Israel.
Rafi EmmanuelMolecular Cell Biology Department, Weizmann Institute of Science, Rehovot, Israel.
Isadora CohenMolecular Cell Biology Department, Weizmann Institute of Science, Rehovot, Israel.
Antonella Di PizioInstitute of Biochemistry, Food Science and Nutrition, The Robert H. Smith Faculty of Agriculture, Food, and Environment, The Hebrew University, Rehovot, Israel.
Jason MadoreMelanoma Institute Australia, University of Sydney, NSW, Australia.
Abdel ElkahlounNational Human Genome Research Institute, US National Institutes of Health, Bethesda, Maryland, USA.
Tamar ZivDepartment of Biology, Technion-Israel Institute of Technology, Haifa, Israel.
Ronen LevyMolecular Cell Biology Department, Weizmann Institute of Science, Rehovot, Israel.
Jared J GartnerNational Cancer Institute, Surgery Branch, US National Institutes of Health, Bethesda, Maryland, 20892, USA.
Victoria K HillNational Human Genome Research Institute, US National Institutes of Health, Bethesda, Maryland, USA.
Jimmy C LinNational Human Genome Research Institute, US National Institutes of Health, Bethesda, Maryland, USA.
Yael HevroniMolecular Cell Biology Department, Weizmann Institute of Science, Rehovot, Israel.
Polina GreenbergMolecular Cell Biology Department, Weizmann Institute of Science, Rehovot, Israel.
Alexandra BrodezkiMolecular Cell Biology Department, Weizmann Institute of Science, Rehovot, Israel.
Steven A RosenbergNational Human Genome Research Institute, US National Institutes of Health, Bethesda, Maryland, USA.
Mickey KosloffDepartment of Human Biology, Faculty of Natural Sciences, University of Haifa, Haifa, Israel.
Nicholas K HaywardMelanoma Institute Australia, University of Sydney, NSW, Australia.
Arie AdmonDepartment of Biology, Technion-Israel Institute of Technology, Haifa, Israel.
Masha Y NivInstitute of Biochemistry, Food Science and Nutrition, The Robert H. Smith Faculty of Agriculture, Food, and Environment, The Hebrew University, Rehovot, Israel.
Richard A ScolyerMelanoma Institute Australia, University of Sydney, NSW, Australia.ORCID http://orcid.org/0000-0002-8991-0013
Kirill A MartemyanovDepartment of Neuroscience, The Scripps Research Institute, FL, 33458, USA.
Yardena SamuelsMolecular Cell Biology Department, Weizmann Institute of Science, Rehovot, Israel. Yardena.Samuels@weizmann.ac.il.
Weizmann Institute of Science · ILNational Institutes of Health · USThe University of Sydney · AUHebrew University of Jerusalem · ILScripps Research Institute · USTechnion – Israel Institute of Technology · ILUniversity of Haifa · IL

Funding

Adoptive Cell Transfer Immunotherapy of CancerZIABC010984 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI ROSENBERG, STEVEN · 2009 to 2025
$56.8M
Gene therapy of cancerZIABC010985 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI ROSENBERG, STEVEN · 2009 to 2025
$56.8M
NHGRI/DIR Microarray CoreZICHG200365 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI ELKAHLOUN, ABDEL · 2011 to 2025
$9.0M
Regulation of Striatal Signaling by RGS ProteinsR01DA036596 · NIDA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Kirill A. Martemyanov · 2014 to 2026
$6.5M
Molecular Basis of RGS Protein Function in the StriatumK02DA026405 · NIDA · UNIVERSITY OF MINNESOTA · PI MARTEMYANOV, KIRILL A. · 2009 to 2019
$1.2M
NIDA NIH HHS K02 DA026405NIDA NIH HHS R01 DA036596
6 · The paper itself

Abstract

Analysis of 501 melanoma exomes revealed RGS7, which encodes a GTPase-accelerating protein (GAP), to be a tumor-suppressor gene. RGS7 was mutated in 11% of melanomas and was found to harbor three recurrent mutations (p.R44C, p.E383K and p.R416Q). Structural modeling of the most common recurrent mutation of the three (p.R44C) predicted that it destabilizes the protein due to the loss of an H-bond and salt bridge network between the mutated position and the serine and aspartic acid residues at positions 58 as 61, respectively. We experimentally confirmed this prediction showing that the p.R44C mutant protein is indeed destabilized. We further show RGS7 p.R44C has weaker catalytic activity for its substrate Gα

Indexed as

MutationCell Line, TumorCell MovementCell ProliferationDisulfidesGTP-Binding Protein alpha Subunits, Gi-GoHumansHydrogen BondingMelanomaModels, MolecularNeoplasm InvasivenessProtein ConformationProtein StabilityRGS ProteinsDisulfidesGTP-Binding Protein alpha Subunits, Gi-GoRGS7 protein, humanRGS Proteins

Identifiers

PMID29330521
PMCPMC5766496
OpenAlexW2783882633

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.