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We have been suggested that AmotP130 suppressed the invasion ability through remodelling of the cytoskeleton of breast cancer cells, involving regulation of the Rho pathway. The cytoskeleton-related pathway components may provide novel, clinically therapeutic targets for breast cancer treatment.
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AMOT, AMOTL1, and AMOTL2 enhance Hippo signaling by stimulating LATS1/2 autophosphorylation and by connecting LATS1/2 with both its activator SAV1-MST1/2 and its substrate YAP.
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AMOT expression is regulated by MiR-4463 in the vascular smooth muscle cell migration.
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Angiomotin promotes prostate cancer cell proliferation by signaling through the Hippo-YAP pathway.
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The authors propose that phosphorylation of Amot(S176) is a critical post-translational modification that suppresses YAP's ability to promote cell proliferation and tumorigenesis by altering the subcellular localization of an essential YAP co-factor.
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Data indicate that Amot is crucial for the maintenance of nuclear YAP to promote renal epithelial and RCC proliferation.
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Decreased AMOT-p130 expression coupled with high nuclear YAP1 expression resulted in shorter overall survival and disease-free survival in patients with advanced gastric cancer.
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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.
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AMOT may function as an oncogene in the progression of colon cancer by activating the YAP-ERK/PI3K-AKT signaling pathway.
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The lncRNA SNHG12 promotes cell proliferation and migration by upregulating AMOT gene expression in osteosarcoma cells in vivo and in vitro.
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angiomotin and Merlin respectively interface cortical actin filaments and core kinases in Hippo signaling
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Study shows miR-205 significantly downregulated and directly target the 3'-UTR of AMOT in breast cancer. In vitro, miR-205 regulates the proliferation and invasion of breast cancer cells through suppression of AMOT expression.
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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.
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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
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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.
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expression is upregulated in sinonasal inverted papilloma
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angiomotin proteins connect F-actin architecture to YAP regulation.
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function of Angiomotins and other members of the Motin protein family
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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.
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Within the nucleus, Amot-p130 was associated with the transcriptional complex containing Yap and Teads (TEA domain family members) and contributed to the regulation of a subset of Yap target genes, many of which are associated with tumorigenesis.