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anti-Human Angiomotin Antibodies:
anti-Mouse (Murine) Angiomotin Antibodies:
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Human Polyclonal Angiomotin Primary Antibody for DB - ABIN1881054
Heller, Adu-Gyamfi, Smith-Kinnaman, Babbey, Vora, Xue, Bittman, Stahelin, Wells: Amot recognizes a juxtanuclear endocytic recycling compartment via a novel lipid binding domain. in The Journal of biological chemistry 2010
Show all 5 Pubmed References
Human Polyclonal Angiomotin Primary Antibody for WB - ABIN531071
Chan, Lim, Chong, Pobbati, Huang, Hong: Hippo pathway-independent restriction of TAZ and YAP by angiomotin. in The Journal of biological chemistry 2011
Show all 2 Pubmed References
Human Polyclonal Angiomotin Primary Antibody for IF (p), IHC (p) - ABIN754873
Shimada, Abe, Kohno, Satohisa, Konno, Takahashi, Hatakeyama, Arimoto, Kakuki, Kaneko, Takano, Saito, Kojima: Loss of tricellular tight junction protein LSR promotes cell invasion and migration via upregulation of TEAD1/AREG in human endometrial cancer. in Scientific reports 2017
Amot and AmotL1 (show AMOTL1 Antibodies) have similar effects on endothelial migration and tight junction formation in vitro. In vivo Amot appears to control the cell polarity and AmotL1 (show AMOTL1 Antibodies) affects the stability of cell-cell junctions.
Thus AMOT is a direct substrate of Lats1 (show LATS1 Antibodies)/2 mediating functions of the Hippo pathway in endothelial cell migration and angiogenesis.
knockdown of Amot reduced the number of filopodia of endoth (show PDPN Antibodies)elial tip cells and severely impaired the migration of intersegmental vessels
Amot and AmotL1 (show AMOTL2 Antibodies) have similar effects on endothelial migration and tight junction formation in vitro. In vivo Amot appears to control the cell polarity and AmotL1 (show AMOTL2 Antibodies) affects the stability of cell-cell junctions.
Decreased AMOT-p130 (show RBL2 Antibodies) expression coupled with high nuclear YAP1 (show YAP1 Antibodies) 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 (show RAB1A Antibodies) in the progression of colon cancer by activating the YAP (show YAP1 Antibodies)-ERK (show EPHB2 Antibodies)/PI3K (show PIK3CA Antibodies)-AKT (show AKT1 Antibodies) 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 (show MLXIP Antibodies)-205 significantly downregulated and directly target the 3'-UTR (show UTS2R Antibodies) of AMOT in breast cancer. In vitro, miR (show MLXIP Antibodies)-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 (show YAP1 Antibodies), YAP (show YAP1 Antibodies)/TAZ (show TAZ Antibodies) and LATS1 (show LATS1 Antibodies).
experiments indicate that AMOT and other motin family members function together with NEDD4L (show NEDD4L Antibodies) 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.
angiomotin proteins connect F-actin architecture to YAP (show YAP1 Antibodies) regulation.
Rho attenuates the interaction between Amot and Nf2 (show NF2 Antibodies) by binding to the coiled-coil domain of Amot.
TFPI-1 (show TFPI Antibodies) interacts with AMOT, which led to a decrease in the phosphorylation of YAP (show YAP1 Antibodies) 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 (show RNF146 Antibodies) 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 (show YAP1 Antibodies) and Teads (TEA domain family members) and contributed to the regulation of a subset of Yap (show YAP1 Antibodies) target genes, many of which are associated with tumorigenesis.
The loss of Angiomotin, together with Angiomotin-like 2 (show AMOTL2 Antibodies), leads to differentiation of inner cell mass cells and compromised peri (show POSTN Antibodies)-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 (show AMOTL1 Antibodies), and Amotl2 (show AMOTL2 Antibodies) are differentially expressed in uterine cells during the peri (show POSTN Antibodies)-implantation period.
A vaccine targeting angiomotin induces an antibody response which alters tumor vessel permeability and hampers the growth of established tumors.
Depletion of Angiomotin in Nf2 (show NF2 Antibodies)(-/-) Schwann cells attenuates the Ras-MAPK (show MAPK1 Antibodies) signaling pathway, impedes cellular proliferation in vitro and tumorigenesis in vivo
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