HECW2, a novel EC ubiquitin E3 ligase, plays a critical role in stabilizing endothelial cell-to-cell junctions by regulating AMOT-like 1 (AMOTL1) stability.
AMOTL1 Promotes Breast Cancer Progression and Is Antagonized by Merlin.
phosphorylation-deficient S793Ala mutant of AMOTL1 showed a shorter half-life and conferred resistance to energy-stress-induced YAP inhibition.
study defined eight additional recurrently mutated genes in SMZL; these genes are CREBBP, CBFA2T3, AMOTL1, FAT4, FBXO11, PLA2G4D, TRRAP and USH2A.
miR-124 binds AmotL1 3'UTR and down-regulates its expression repressing vasculogenic mimicry and cell motility in cervical cancer cells.
Scaffold proteins angiomotin (Amot) and angiomotin-related AmotL1 and AmotL2 were recently identified as negative regulators of YAP and TAZ by preventing their nuclear translocation.
These results suggested that IFN-gamma exhibits anti-angiogenesis effects by regulating the expression of TNF-alpha-induced AmotL1 via NFkappaB in emphysema lungs.
AmotL1 and ZO-2 are two candidates that could be harnessed to control the oncogenic function of YAP.
By yeast two-hybrid screening, angiomotin-like 1 (AmotL1) was identified as a host factor that interacts with the M protein of parainfluenza virus 5 (PIV5).
The angiomotin-like 1 is involved in actin-cytoskeleton-based processes, in part, via its interaction with a p80-angiomotin-containing complex and the actin cytoskeleton
Amot and AmotL1 have similar effects on endothelial migration and tight junction formation in vitro. In vivo Amot appears to control the cell polarity and AmotL1 affects the stability of cell-cell junctions.
Amot and AmotL1 have similar effects on endothelial migration and tight junction formation in vitro. In vivo Amot appears to control the cell polarity and AmotL1 affects the stability of cell-cell junctions.
Fat4 is not required for the canonical activation of Hippo kinases but it sequesters a partner of Yap1, Amotl1, out of the nucleus.
The authors propose that AmotL1 is an essential effector of the N-cadherin mediated endothelial/pericyte junctional complex.
These results suggested that IFN-gamma exhibits anti-angiogenesis effects by regulating the expression of TNF-alpha-induced AmotL1 via NFkappaB in emphysema lungs.
Amot, Amotl1, and Amotl2 are differentially expressed in uterine cells during the peri-implantation period.
Data show that MUPP1 interacts with angiomotin (Amot), JEAP/Amot-like 1 and MASCOT/Amot-like 2, and that all the Amot/JEAP family proteins also interacted with Patj, a close relative of MUPP1.
Amot and AmotL1 have similar effects on endothelial migration and tight junction formation in vitro. In vivo Amot appears to control the cell polarity and AmotL1 affects the stability of cell-cell junctions.
The protein encoded by this gene is a peripheral membrane protein that is a component of tight junctions or TJs. TJs form an apical junctional structure and act to control paracellular permeability and maintain cell polarity. This protein is related to angiomotin, an angiostatin binding protein that regulates endothelial cell migration and capillary formation.
angiomotin like 1 , angiomotin-like protein 1-like , angiomotin-like protein 1 , junction-enriched and associated protein , junction-enriched and -associated protein
GENE ID | SPEZIES |
---|---|
100513610 | Sus scrofa |
154810 | Homo sapiens |
485122 | Canis lupus familiaris |
541209 | Bos taurus |
75723 | Mus musculus |
315430 | Rattus norvegicus |