[Molecular basis of Hirschsprung disease].

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

Back to search

Article

[Molecular basis of Hirschsprung disease].

Nihon rinsho. Japanese journal of clinical medicine - 1 Jan 1998

Inoue M, Okada A

Abstract excerpt

Hirschsprung disease (HSCR) is a congenital malformation caused by the absence of ganglion cells in the myenteric and submucosal plexuses of the gut. Recent studies have shown that mutations in the RET, glial-cell-derived neurotrophic factor (GDNF), endothelin-B receptor (EDNRB), endothelin-3 gen...

Topics

Animals
Drosophila Proteins
Endothelin-3
Glial Cell Line-Derived Neurotrophic Factor
Glial Cell Line-Derived Neurotrophic Factor Receptors
Hirschsprung Disease
Humans
Mutation
Nerve Growth Factors
Nerve Tissue Proteins
Proto-Oncogene Proteins
Proto-Oncogene Proteins c-kit
Proto-Oncogene Proteins c-ret
Receptor Protein-Tyrosine Kinases
Receptor, Endothelin B
Receptors, Endothelin
Signal Transduction

Source

Open in PubMed

Identifiers

PMID: 9465697

Genes

RET
EDNRB
GDNF

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 30 Aug 2026. Prepared record publication-9465697-2026-08-30.1. Manifest publication-graph-cohort-2026-08-30.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 30 Aug 2026.

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

discussions

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics