Emerging roles for angiomotin in the nervous system.
Angiomotins
Cell Movement
Dendrites
/ metabolism
Hippo Signaling Pathway
Humans
Intercellular Signaling Peptides and Proteins
/ metabolism
Microfilament Proteins
/ metabolism
Neurogenesis
Protein Isoforms
/ metabolism
Protein Serine-Threonine Kinases
/ metabolism
Signal Transduction
Synapses
/ metabolism
Journal
Science signaling
ISSN: 1937-9145
Titre abrégé: Sci Signal
Pays: United States
ID NLM: 101465400
Informations de publication
Date de publication:
27 10 2020
27 10 2020
Historique:
entrez:
28
10
2020
pubmed:
29
10
2020
medline:
9
11
2021
Statut:
epublish
Résumé
Angiomotins are a family of molecular scaffolding proteins that function to organize contact points (called tight junctions in vertebrates) between adjacent cells. Some angiomotin isoforms bind to the actin cytoskeleton and are part of signaling pathways that influence cell morphology and migration. Others cooperate with components of the Hippo signaling pathway and the associated networks to control organ growth. The 130-kDa isoform, AMOT-p130, has critical roles in neural stem cell differentiation, dendritic patterning, and synaptic maturation-attributes that are essential for normal brain development and are consistent with its association with autism. Here, we review and discuss the evidence that supports a role for AMOT-p130 in neuronal development in the central nervous system.
Identifiants
pubmed: 33109746
pii: 13/655/eabc0635
doi: 10.1126/scisignal.abc0635
pii:
doi:
Substances chimiques
AMOT protein, human
0
Angiomotins
0
Intercellular Signaling Peptides and Proteins
0
Microfilament Proteins
0
Protein Isoforms
0
Protein Serine-Threonine Kinases
EC 2.7.11.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : CIHR
ID : MOP 84366
Pays : Canada
Organisme : CIHR
ID : PJT 159738
Pays : Canada
Informations de copyright
Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.