Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Exploring the effect of D61G mutation on SHP2 cause gain of function activity by a molecular dynamics study.

Journal of biomolecular structure & dynamics - 1 Nov 2018

Li Hong-Lian, Ma Ying, Zheng Chang-Jie, Jin Wen-Yan, Liu Wen-Shan, Wang Run-Ling

Abstract excerpt

Noonan syndrome (NS) is a common autosomal dominant congenital disorder which could cause the congenital cardiopathy and cancer predisposition. Previous studies reported that the knock-in mouse models of the mutant D61G of SHP2 exhibited the major features of NS, which demonstrated that the mutation D61G of SHP2 could cause NS. To explore the effect of D61G mutation on SHP2 and explain the high activity of the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Enzyme Stability
Share to Gain of Function Mutation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hydrogen Bonding

Share to Molecular Conformation

Share to Molecular Dynamics Simulation

Share to Protein Interaction Domains and Motifs

Share to Protein Tyrosine Phosphatase, Non-Receptor Type 11

Share to Structure-Activity Relationship

Source

Identifiers

PMID: 29125030
DOI: 10.1080/07391102.2017.1402709

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Exploring the effect of D61G mutation on SHP2 cause gain of function activity by a molecular dynamics study.PMID 29125030Read ↗

SHP2 clinical phenotype, cancer, or RASopathies, can be predicted by mutant conformational propensities.Semantic proximity Read ↗

[The Biological Function of SHP2 in Human Disease].Semantic proximity Read ↗

Unraveling the molecular effects of mutation L270P on Wiskkot-Aldrich syndrome protein: insights from molecular dynamics approach.Semantic proximity Read ↗

Unveiling conformational dynamics changes of H-Ras induced by mutations based on accelerated molecular dynamics.Semantic proximity Read ↗

Probing the Effect of Two Heterozygous Mutations in Codon 723 of SLC26A4 on Deafness Phenotype Based on Molecular Dynamics Simulations.Semantic proximity Read ↗

Impact of disease-causing mutations on inter-domain interactions in cMyBP-C: a steered molecular dynamics study.Semantic proximity Read ↗

Gain-of-function mutations in the gene encoding the tyrosine phosphatase SHP2 induce hydrocephalus in a catalytically dependent manner.Semantic proximity Read ↗

Unveiling the Molecular Basis of the Noonan Syndrome-Causing Mutation T42A of SHP2.Semantic proximity Read ↗

The pathogenic E139D mutation stabilizes a non-canonical active state of the multi-domain phosphatase SHP2Semantic proximity Read ↗

The pathogenic E139D mutation stabilizes a non-canonical active state of the multi-domain phosphatase SHP2.Semantic proximity Read ↗

Investigation of binding phenomenon of NSP3 and p130Cas mutants and their effect on cell signalling.Semantic proximity Read ↗

The two mutations of actin-myosin interface and their effect on the dynamics, structures, and functions of skeletal muscle actin.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.