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

Effect of disease-associated SLC9A9 mutations on protein–protein interaction networks: implications for molecular mechanisms for ADHD and autism

1 Mar 2019

Abstract excerpt

No abstract is available from the source.

Read the complete abstract on PubMed

Topics

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

Share to Attention Deficit Hyperactivity Disorder
Share to Genetics and Neurodevelopmental Disorders
Share to Pancreatic function and diabetes

Source

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 30927234
DOI: 10.1007/s12402-018-0281-x

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Effect of disease-associated SLC9A9 mutations on protein–protein interaction networks: implications for molecular mechanisms for ADHD and autismPMID 30927234Read ↗

SLC9A9 mutations, gene expression, and protein-protein interactions in rat models of attention-deficit/hyperactivity disorder.Semantic proximity Read ↗

Sodium hydrogen exchanger 9 NHE9 (SLC9A9) and its emerging roles in neuropsychiatric comorbidity.Semantic proximity Read ↗

Pathogenic mechanisms underlying SLC6A1 variant-mediated neurodevelopmental disorders.Semantic proximity Read ↗

An interactome perturbation framework prioritizes damaging missense mutations for developmental disorders.Semantic proximity Read ↗

Landscape of Intrinsically Disordered Proteins in Mental Disorder DiseasesSemantic proximity Read ↗

The contribution of protein intrinsic disorder to understand the role of genetic variants uncovered by autism spectrum disorders exome studies.Semantic proximity Read ↗

De novo variants in NPTN cause a neurodevelopmental disorder with autism and neuroplastin-PMCA hypofunctionSemantic proximity Read ↗

The solute carrier superfamily interactomeSemantic proximity Read ↗

Autism-associated PTCHD1 missense variants bind to the SNARE-associated protein, SNAPIN, but exhibit impaired subcellular traffickingSemantic proximity Read ↗

A low frequency damaging SORCS2 variant identified in a family with ADHD compromises receptor stability and quenches activity.Semantic proximity Read ↗

Functional evaluation of autism-associated mutations in NHE9.Semantic proximity Read ↗

Single nucleotide variations encoding missense mutations in G protein-coupled receptors may contribute to autism.Semantic proximity Read ↗

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