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

Isolation and characterisation of the chick orthologue of the Opitz syndrome gene, Mid1, supports a conserved role in vertebrate development.

The International journal of developmental biology - 1 Jan 2002

Richman Joy M, Fu Katherine K, Cox Liza L, Sibbons Jane P, Cox Timothy C

Abstract excerpt

The X-linked form of Opitz syndrome (OS) is caused by loss of function of the microtubule-associated MID1 protein. The phenotype of OS includes defects along the central body axis, namely hypertelorism, cleft lip and palate, hypospadias and cardiac structural anomalies. Here we describe the isolation and characterisation of full-length cDNA clones representing the chick Mid1 gene and the detailed profile of its...

Read the complete abstract on PubMed

Topics

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

Share to Chick Embryo
Share to High Mobility Group Proteins

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Ligases

Share to Mesoderm

Share to Microtubule Proteins

Share to Neural Crest

Share to Prosencephalon

Share to SOXE Transcription Factors

Source

Identifiers

PMID: 12141430

Genes

MID1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Isolation and characterisation of the chick orthologue of the Opitz syndrome gene, Mid1, supports a conserved role in vertebrate development.PMID 12141430Read ↗

Evidence of functional redundancy between MID proteins: implications for the presentation of Opitz syndrome.Semantic proximity Read ↗

The MID1 protein is a central player during development and in disease.Semantic proximity Read ↗

Opitz G/BBB syndrome, a defect of midline development, is due to mutations in a new RING finger gene on Xp22.Semantic proximity Read ↗

Functional characterization of the Opitz syndrome gene product (midin): evidence for homodimerization and association with microtubules throughout the cell cycle.Semantic proximity Read ↗

Detailed analysis of chick optic fissure closure reveals Netrin-1 as an essential and conserved mediator of epithelial fusion during vertebrate embryogenesisSemantic proximity Read ↗

X-linked Opitz syndrome: novel mutations in the MID1 gene and redefinition of the clinical spectrum.Semantic proximity Read ↗

The mouse Mid1 gene: implications for the pathogenesis of Opitz syndrome and the evolution of the mammalian pseudoautosomal regionSemantic proximity Read ↗

The Opitz syndrome gene product, MID1, associates with microtubules.Semantic proximity Read ↗

New mutations in MID1 provide support for loss of function as the cause of X-linked Opitz syndrome.Semantic proximity Read ↗

Isolation of the chicken Lmbr1 coding sequence and characterization of its role during chick limb development.Semantic proximity Read ↗

Exon 2 duplication of the MID1 gene in a patient with a mild phenotype of Opitz G/BBB syndrome.Semantic proximity Read ↗

Studies of the tissues and molecules that regulate the migration of cranial neural crest cells in the chicken embryo : roles of Midline 1 and retinoic acidSemantic proximity Read ↗

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