Evidence map›Paper›PMID 32187889›Full record

ArticleBirth defects research2020

GTP hydrolysis is modulated by Arg34 in the RASopathy-associated KRAS

Asim K Bera, Jia Lu, Chunya Lu, Lianbo Li, Sudershan Gondi, Wei Yan, Andrew Nelson, Goujun Zhang, Kenneth D Westover

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Birth defects research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 44% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
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

9 authors at 3 institutions in 2 countries.

Asim K BeraDepartment of Biochemistry and Radiation Oncology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas.
Jia LuDepartment of Biochemistry and Radiation Oncology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas.
Chunya LuDepartment of Biochemistry and Radiation Oncology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas.
Lianbo LiDepartment of Biochemistry and Radiation Oncology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas.
Sudershan GondiDepartment of Biochemistry and Radiation Oncology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas.
Wei YanDepartment of Biochemistry and Radiation Oncology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas.
Andrew NelsonBrigham Young University, Provo, Utah.
Goujun ZhangDepartment of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Kenneth D WestoverDepartment of Biochemistry and Radiation Oncology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas.ORCID 0000-0003-3653-5923
The University of Texas Southwestern Medical Center · USFirst Affiliated Hospital of Zhengzhou University · CNBrigham Young University · US

Funding

Project 4: Secondary Cancers Among NF1 Cancer SurvivorsU54CA196519 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI Yunlong Liu · 2015 to 2026
$26.9M
NCI NIH HHS U54 CA196519
6 · The paper itself

Abstract

RAS proteins are commonly mutated in cancerous tumors, but germline RAS mutations are also found in RASopathy syndromes such as Noonan syndrome (NS) and cardiofaciocutaneous (CFC) syndrome. Activating RAS mutations can be subclassified based on their activating mechanisms. Understanding the structural basis for these mechanisms may provide clues for how to manage associated health conditions. We determined high-resolution X-ray structures of the RASopathy mutant KRAS

Indexed as

Noonan SyndromeProto-Oncogene Proteins p21(ras)ras ProteinsGuanosine TriphosphateHumansHydrolysisGuanosine TriphosphateKRAS protein, humanProto-Oncogene Proteins p21(ras)ras ProteinsCFC syndromeGAP-insensitiveGTPaseNoonan syndromeRAS

Identifiers

PMID32187889
PMCPMC7495839
OpenAlexW3011616287

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.