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Amot and AmotL1 (zeige AMOTL1 ELISA Kits) have similar effects on endothelial migration and tight junction formation in vitro. In vivo Amot appears to control the cell polarity and AmotL1 (zeige AMOTL1 ELISA Kits) affects the stability of cell-cell junctions.
Thus AMOT is a direct substrate of Lats1/2 mediating functions of the Hippo pathway in endothelial cell migration and angiogenesis.
knockdown of Amot reduced the number of filopodia of endoth (zeige PDPN ELISA Kits)elial tip cells and severely impaired the migration of intersegmental vessels
Amot and AmotL1 (zeige AMOTL2 ELISA Kits) have similar effects on endothelial migration and tight junction formation in vitro. In vivo Amot appears to control the cell polarity and AmotL1 (zeige AMOTL2 ELISA Kits) affects the stability of cell-cell junctions.
Data indicate that Amot is crucial for the maintenance of nuclear YAP (zeige YAP1 ELISA Kits) to promote renal epithelial and RCC (zeige XRCC1 ELISA Kits) proliferation.
Decreased AMOT-p130 (zeige RBL2 ELISA Kits) expression coupled with high nuclear YAP1 (zeige YAP1 ELISA Kits) expression resulted in shorter overall survival and disease-free survival in patients with advanced gastric cancer.
Study focused on the methylation profile of the AMOT promoter CpG island during development, comparing it in circulating cord blood endothelial progenitor cells (ECFC) of cord blood from term versus preterm newborns. Findings highlight importance of pro-angiogenic AMOT gene methylation in ECFC, suggesting that epigenetic mechanisms may control the regulation of angiogenesis during development.
AMOT may function as an oncogene (zeige RAB1A ELISA Kits) in the progression of colon cancer by activating the YAP (zeige YAP1 ELISA Kits)-ERK (zeige EPHB2 ELISA Kits)/PI3K (zeige PIK3CA ELISA Kits)-AKT (zeige AKT1 ELISA Kits) signaling pathway.
The lncRNA SNHG12 promotes cell proliferation and migration by upregulating AMOT gene expression in osteosarcoma cells in vivo and in vitro.
angiomotin and Merlin respectively interface cortical actin filaments and core kinases in Hippo signaling
Study shows miR (zeige MLXIP ELISA Kits)-205 significantly downregulated and directly target the 3'-UTR (zeige UTS2R ELISA Kits) of AMOT in breast cancer. In vitro, miR (zeige MLXIP ELISA Kits)-205 regulates the proliferation and invasion of breast cancer cells through suppression of AMOT expression.
Amot was highly expressed in breast cancer tissues and was important in the promotion of breast cancer cell proliferation and invasion. Amot knockdown in MCF-7 cells decreased the expression of YAP, YAP/TAZ and LATS1.
experiments indicate that AMOT and other motin family members function together with NEDD4L to help complete immature virion assembly prior to ESCRT-mediated virus budding
AMOT is a crucial suppressor of lung cancer metastasis and highlight its critical role as a tumor suppressor and its potential as a prognostic biomarker and therapeutic target for lung cancer.
Collectively, we have uncovered that AMOT acts as a YAP (zeige YAP1 ELISA Kits) stimulator in high glucose level.
Rho attenuates the interaction between Amot and Nf2 (zeige NF2 ELISA Kits) by binding to the coiled-coil domain of Amot.
TFPI-1 (zeige TFPI ELISA Kits) interacts with AMOT, which led to a decrease in the phosphorylation of YAP (zeige YAP1 ELISA Kits) and further increased the genes expression of the proliferation and migration involved. Our results further confirmed that atherosclerosis was a localized disease.
a new function of RNF146 (zeige RNF146 ELISA Kits) and tankyrase in stabilizing the Crumbs complex through downregulation of AMOT proteins at the apical membrane, is reported.
Within the nucleus, Amot-p130 was associated with the transcriptional complex containing Yap (zeige YAP1 ELISA Kits) and Teads (TEA domain family members) and contributed to the regulation of a subset of Yap (zeige YAP1 ELISA Kits) target genes, many of which are associated with tumorigenesis.
The loss of Angiomotin, together with Angiomotin-like 2 (zeige AMOTL2 ELISA Kits), leads to differentiation of inner cell mass cells and compromised peri (zeige POSTN ELISA Kits)-implantation development.
The phosphorylation of S176 in the N-terminal domain of Amot is a critical step for activation of the Hippo pathway in adherens junctions and cell polarity disconnects the Hippo pathway from cell-cell adhesion by sequestering Amot from AJs.
Amot, Amotl1 (zeige AMOTL1 ELISA Kits), and Amotl2 (zeige AMOTL2 ELISA Kits) are differentially expressed in uterine cells during the peri (zeige POSTN ELISA Kits)-implantation period.
A vaccine targeting angiomotin induces an antibody response which alters tumor vessel permeability and hampers the growth of established tumors.
This gene belongs to the motin family of angiostatin binding proteins characterized by conserved coiled-coil domains and C-terminal PDZ binding motifs. The encoded protein is expressed predominantly in endothelial cells of capillaries as well as larger vessels of the placenta where it may mediate the inhibitory effect of angiostatin on tube formation and the migration of endothelial cells toward growth factors during the formation of new blood vessels. Alternative splicing results in multiple transcript variants encoding different isoforms.
angiomotin like 2
, angiomotin-like protein 2
, angiomotin-like protein 2-like
, angiomotin p130 isoform
, angiomotin p80 isoform