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

Zebrafish model of holoprosencephaly demonstrates a key role for TGIF in regulating retinoic acid metabolism.

Human molecular genetics - 15 Feb 2008

Gongal Patricia A, Waskiewicz Andrew J

Abstract excerpt

Holoprosencephaly (HPE) is the most common human congenital forebrain defect, affecting specification of forebrain tissue and subsequent division of the cerebral hemispheres. The causes of HPE are multivariate and heterogeneous, and include exposure to teratogens, such as retinoic acid (RA), and mutations in forebrain patterning genes. Many of the defects in HPE patients resemble animal models with aberrant RA...

Read the complete abstract on PubMed

Topics

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

Share to Body Patterning
Share to Genes, Homeobox
Share to Holoprosencephaly

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Oligodeoxyribonucleotides, Antisense

Share to Prosencephalon

Share to Rhombencephalon

Share to Tretinoin

Share to Zebrafish Proteins

Source

Identifiers

PMID: 17998248
DOI: 10.1093/hmg/ddm328

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

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

Zebrafish model of holoprosencephaly demonstrates a key role for TGIF in regulating retinoic acid metabolism.PMID 17998248Read ↗

Folic acid prevention of neural tube defects requires retinoic acid produced by ALDH1L1Semantic proximity Read ↗

Craniosynostosis and Multiple Skeletal Anomalies in Humans and Zebrafish Result from a Defect in the Localized Degradation of Retinoic AcidSemantic proximity Read ↗

Loss of Tgif function causes holoprosencephaly by disrupting the SHH signaling pathway.Semantic proximity Read ↗

Intragenic deletion of Tgif causes defectsin brain development.Semantic proximity Read ↗

Exogenous retinoic acid during gastrulation induces cartilaginous and other craniofacial defects in Fundulus heteroclitus.Semantic proximity Read ↗

Mutations in holoprosencephaly.Semantic proximity Read ↗

Impact of retinoic acid exposure on midfacial shape variation and manifestation of holoprosencephaly in Twsg1 mutant mice.Semantic proximity Read ↗

Forebrain induction, retinoic acid, and vulnerability to schizophrenia: insights from molecular and genetic analysis in developing mice.Semantic proximity Read ↗

Functions of TGIF homeodomain proteins and their roles in normal brain development and holoprosencephaly.Semantic proximity Read ↗

Local retinoid signaling coordinates forebrain and facial morphogenesis by maintaining FGF8 and SHHSemantic proximity Read ↗

Ethanol induces embryonic malformations by competing for retinaldehyde dehydrogenase activity during vertebrate gastrulation.Semantic proximity Read ↗

Insights into retinoic acid deficiency and the induction of craniofacial malformations and microcephaly in fetal alcohol spectrum disorderSemantic proximity Read ↗

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