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

Trio cooperates with Myh9 to regulate neural crest-derived craniofacial development.

Theranostics - 1 Jan 2021

Guo Shuyu, Meng Li, Liu Haojie, Yuan Lichan, Zhao Na, Ni Jieli, Zhang Yang, Ben Jingjing, Li Yi-Ping, Ma Junqing

Abstract excerpt

Trio is a unique member of the Rho-GEF family that has three catalytic domains and is vital for various cellular processes in both physiological and developmental settings. TRIO mutations in humans are involved in craniofacial abnormalities, in which patients present with mandibular retrusion. However, little is known about the molecular mechanisms of Trio in neural crest cell (NCC)-derived craniofacial...

Read the complete abstract on PubMed

Topics

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

Share to beta Catenin
Share to Cell Movement
Share to Embryo, Mammalian

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

Share to Gene Expression Regulation, Developmental

Share to HEK293 Cells

Share to Myosin Heavy Chains

Share to Neural Crest

Share to Zebrafish

Source

Open in PubMed Open full text

Identifiers

PMID: 33754063
DOI: 10.7150/thno.51745
PMCID: PMC7977452

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. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Trio cooperates with Myh9 to regulate neural crest-derived craniofacial development.PMID 33754063Read ↗

The Rho guanine nucleotide exchange factor Trio is required for neural crest cell migration and interacts with Dishevelled.Semantic proximity Read ↗

Skeletal muscle deformity and neuronal disorder in Trio exchange factor-deficient mouse embryos.Semantic proximity Read ↗

The Human Rho-GEF trio and its target GTPase RhoG are involved in the NGF pathway, leading to neurite outgrowth.Semantic proximity Read ↗

Opposite Modulation of RAC1 by Mutations in TRIO Is Associated with Distinct, Domain-Specific Neurodevelopmental Disorders.Semantic proximity Read ↗

Dosage-sensitive, reciprocal genetic interactions between the Abl tyrosine kinase and the putative GEF trio reveal trio's role in axon pathfinding.Semantic proximity Read ↗

The trio guanine nucleotide exchange factor is a RhoA target. Binding of RhoA to the trio immunoglobulin-like domain.Semantic proximity Read ↗

The UNC-73/Trio RhoGEF-2 domain is required in separate isoforms for the regulation of pharynx pumping and normal neurotransmission in C. elegans.Semantic proximity Read ↗

Genetic variants linked to neurodevelopmental disorders within the β3-β4 loop of the TRIO PH2 domain release autoinhibition of GEF2 activitySemantic proximity Read ↗

Rho-GEF Trio regulates osteosarcoma progression and osteogenic differentiation through Rac1 and RhoASemantic proximity Read ↗

Modeling human mutations to understand TRIO GEF function during development.Semantic proximity Read ↗

TRIO loss of function is associated with mild intellectual disability and affects dendritic branching and synapse function.Semantic proximity Read ↗

The RNA binding protein Nab2 regulates splicing of the RhoGEF <i>trio</i> transcript to govern axon and dendrite morphologySemantic proximity Read ↗

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