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Our data suggest that screening for large RASA1 deletions and duplications in this disorder is important and suggest that NGS multi-gene panel testing is beneficial for the molecular diagnosis of cases with complex vascular phenotypes.
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Study found that RASA1, a known target of miR-132, was downregulated in human dermal fibroblasts upon miR-132 overexpression which contributes to the pro-migratory function of miR-132 in fibroblasts.
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miR21 regulated cell proliferation, migration, invasion and tumor growth of esophageal squamous cell carcinoma by directly targeting RASA1, which may have been achieved via regulation of Snail and vimentin.
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A somatic RASA1 mutation in addition to the germline RASA1 mutation, was detected within endothelial cells in capillary malformation-arteriovenous malformation.
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RASA1 variants are rarely found in children with sporadic capillary malformations of lower limbs without capillary malformation-arteriovenous malformation syndrome.
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we demonstrated a novel oncogenic mechanism of PTP1B on affecting PITX1/p120RasGAP in colorectal carcinoma(CRC). Regorafenib inhibited CRC survival through reserving PTP1B-dependant PITX1/p120RasGAP downregulation. PTP1B may be a potential biomarker predicting regorafenib effectiveness, and a potential solution for CRC
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RASA1 mutations are associated melanoma tumorigenesis.
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MicroRNA-21 reduces RASA1 expression in cervical cancer cell lines and promotes cervical cancer cell migration via RASA1. Furthermore, Ras-induced epithelial-mesenchymal transition contributes to miR-21/RASA1 axis promoting cervical cancer cell migration.
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These results and the extreme variable expressivity support the hypothesis that somatic "second hits" are required for the development of vascular anomalies associated with CM-AVM syndrome. In addition, the phenotypes of the affected individuals further clarify that lymphatic manifestations are also part of the phenotypic spectrum of RASA1-related disorders.
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results indicate that, mTOR, Bad, or Survivin are not required for p120 RasGAP fragment N to protect cells from cell death; conclude that downstream targets of Akt other than mTORC1, Bad, or survivin mediate fragment N-induced protection or that several Akt effectors can compensate for each other to induce the pro-survival fragment N-dependent responses
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The interaction between RASA1 and EPHB4 is an indication of the major cause of capillary malformation with arteriovenous malformation.
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Low RASA1 expression is associated with Triple-Negative Breast Cancer.
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QKI-5 stabilized RASA1 mRNA via directly binding to the QKI response element region of RASA1, which in turn prevented the activation of the Ras-MAPK signaling pathway, suppressed cellular proliferation and induced cell cycle arrest.
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Data show that patients with low level of Ras GTPase-activating protein 1 (RASA1) expression correlated with a significantly poorer survival compared to those with high level of RASA1 expression.
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Results show that oncogenic KRAS can activate Rho through miR-31-mediated regulation of RASA1 indicating miR-31 acts as a KRAS effector to modulate invasion and migration in pancreatic cancer.
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PTP1B dephosphorylates PITX1 to weaken its protein stability and the transcriptional activity for p120RasGAP gene expression
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Data suggest that, in response to netrin-1/netrin receptor (DCC) signaling, p120RasGAP is recruited to growth cones and supports axon outgrowth; p120RasGAP Src homology 2 domains exhibit scaffolding properties sufficient to support axon outgrowth.
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Maternal and fetal capillary malformation-arteriovenous malformation due to a novel RASA1 mutation presenting with prenatal non-immune hydrops fetalis have been found.
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This is the second largest study on isolated, non-syndromic Port-wine stain; data suggest that GNAQ is the main genetic determinant in this condition. Moreover, isolated port-wine stains are distinct from capillary malformations seen in RASA1 disorders.
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Data showed that hypoxia regulated the expression of miR-182 and RASA1 to promote HCC angiogenesis.
