Evidence map›Paper›PMID 28154176›Full record

ArticleThe Journal of biological chemistry2017

A KRAS GTPase K104Q Mutant Retains Downstream Signaling by Offsetting Defects in Regulation.

Guowei Yin, Samantha Kistler, Samuel D George, Nora Kuhlmann, Leslie Garvey, Minh Huynh, Rachel K Bagni, Michael Lammers, Channing J Der, Sharon L Campbell

Open access · hybridAbstract read
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 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.0field-weighted citation impact, top 13% 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, 46 citations in OpenAlex.

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  15. The Importance of MgChemistry (Weinheim an der Bergstrasse, Germany) · 2022
    Article
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  19. Post-translational modification of RAS proteins.Current opinion in structural biology · 2021
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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

10 authors at 3 institutions in 3 countries.

Guowei YinFrom the Department of Biochemistry and Biophysics.ORCID 0000-0003-2669-7160
Samantha KistlerFrom the Department of Biochemistry and Biophysics.
Samuel D GeorgeDepartment of Pharmacology, and.
Nora Kuhlmannthe Institute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-associated Diseases (CECAD), Joseph-Stelzmann-Strasse 26, University of Cologne, 50931 Cologne, Germany, and.
Leslie Garveythe NCI RAS Initiative, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Frederick, Maryland 21702.
Minh HuynhFrom the Department of Biochemistry and Biophysics.
Rachel K Bagnithe NCI RAS Initiative, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Frederick, Maryland 21702.
Michael Lammersthe Institute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-associated Diseases (CECAD), Joseph-Stelzmann-Strasse 26, University of Cologne, 50931 Cologne, Germany, and.
Channing J DerDepartment of Pharmacology, and.
Sharon L CampbellFrom the Department of Biochemistry and Biophysics, campbesl@med.unc.edu.
University of North Carolina at Chapel Hill · USFrederick National Laboratory for Cancer Research · USUniversity of Cologne · DE

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Deborah F. Tate · 1985 to 2026
$201.5M
Project 4: The role of codon bias in RAS tumorigenesisP01CA203657 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI COUNTER, CHRISTOPHER M · 2016 to 2020
$7.9M
BIOLOGICAL ACTIVITY OF RAS ONCOGENESR01CA042978 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 1986 to 2017
$5.9M
MOLECULAR AND CELLULAR BIOPHYSICS TRAINING PROGRAMT32GM008570 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KUHLMAN, BRIAN A, SLEP, KEVIN C · 1995 to 2022
$5.1M
Identification of synthetic lethal interactors in pancreatic cancerU01CA199235 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI COX, ADRIENNE D, DER, CHANNING J. · 2015 to 2019
$2.5M
Regulation of Ras by MonoubiquitinationR01GM106227 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CAMPBELL, SHARON L · 2013 to 2016
$1.5M
NCI NIH HHS P01 CA203657NCI NIH HHS P30 CA016086NCI NIH HHS R01 CA042978NCI NIH HHS U01 CA199235NIGMS NIH HHS R01 GM106227NIGMS NIH HHS T32 GM008570
6 · The paper itself

Abstract

The KRAS GTPase plays a critical role in the control of cellular growth. The activity of KRAS is regulated by guanine nucleotide exchange factors (GEFs), GTPase-activating proteins (GAPs), and also post-translational modification. Lysine 104 in KRAS can be modified by ubiquitylation and acetylation, but the role of this residue in intrinsic KRAS function has not been well characterized. We find that lysine 104 is important for GEF recognition, because mutations at this position impaired GEF-mediated nucleotide exchange. Because the KRAS K104Q mutant has recently been employed as an acetylation mimetic, we conducted a series of studies to evaluate its

Indexed as

Mutation, MissenseAnimalsCells, CulturedGuanine Nucleotide Exchange FactorsGuanosine TriphosphateHumansHydrolysisMiceModels, MolecularNIH 3T3 CellsPoint MutationProtein ConformationProtein StabilityProto-Oncogene Proteins p21(ras)Signal TransductionGuanine Nucleotide Exchange FactorsGuanosine TriphosphateHras protein, mouseKRAS protein, humanProto-Oncogene Proteins p21(ras)GTPase-activating protein (GAP)guanine nucleotide exchange factor (GEF)nuclear magnetic resonance (NMR)post-translational modificationprotein acetylationRas proteinsignalingtumorigenesis

Identifiers

PMID28154176
PMCPMC5377764
OpenAlexW2581362192

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.