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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 (show MLXIP Proteins)-21/RASA1 axis promoting cervical cancer cell migration.
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.
results indicate that, mTOR (show FRAP1 Proteins), Bad, or Survivin (show BIRC5 Proteins) are not required for p120 RasGAP fragment N to protect cells from cell death; conclude that downstream targets of Akt (show AKT1 Proteins) other than mTORC1, Bad, or survivin (show BIRC5 Proteins) mediate fragment N-induced protection or that several Akt (show AKT1 Proteins) effectors can compensate for each other to induce the pro-survival fragment N-dependent responses
The interaction between RASA1 and EPHB4 (show EPHB4 Proteins) is an indication of the major cause of capillary malformation with arteriovenous malformation.
Low RASA1 expression is associated with Triple-Negative Breast Cancer.
QKI-5 (show QKI Proteins) stabilized RASA1 mRNA via directly binding to the QKI (show QKI Proteins) response element region of RASA1, which in turn prevented the activation of the Ras-MAPK (show MAPK1 Proteins) signaling pathway, suppressed cellular proliferation and induced cell cycle arrest.
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.
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.
PTP1B (show PTPN1 Proteins) dephosphorylates PITX1 (show PITX1 Proteins) to weaken its protein stability and the transcriptional activity for p120RasGAP gene expression
Data suggest that, in response to netrin-1 (show NTN1 Proteins)/netrin receptor (DCC (show DCC Proteins)) signaling, p120RasGAP is recruited to growth cones and supports axon outgrowth; p120RasGAP Src (show SRC Proteins) homology 2 domains exhibit scaffolding properties sufficient to support axon outgrowth.
The data suggest that nitrosylation of H-Ras (show HRAS Proteins) rearranges the adsorptive potential and intrinsic GTPase (show RACGAP1 Proteins) activity of H-Ras (show HRAS Proteins) through modification of C-terminal cysteines of molecule.
RASA1 catalytic activity is essential for the function and development of lymphatic vessel valves.
These results indicate that the caspase-3 (show CASP3 Proteins)/p120 RasGAP stress-sensing module impacts on carcinogen-induced liver cancer incidence but not sufficiently so as to affect overall survival.
Double-deficient RASA1-neurofibromin 1 (show NF1 Proteins) mice developed T cell acute lymphoblastic leukemia/lymphoma, which originated at an early point in T cell development and was dependent on activating mutations in the Notch1 (show NOTCH1 Proteins) gene.
Rasa1 may have a role in pathogenesis of capillary malformation-arteriovenous malformation in a mouse model
Regulation of Rasa1 translation by miR (show MLXIP Proteins)-132 was seen in severed axons, demonstrating local function within the axon.
RASA1 mutation is responsible for the aberrant lymphatic architecture and functional abnormalities, as visualized in the PKWS subject and in the animal model.
MicroRNA-31 activates the RAS pathway and functions as an oncogenic MicroRNA by repressing RAS p21 GTPase activating protein 1 (RASA1)
14-3-3 (show YWHAQ Proteins) negatively regulates the RGC downstream of the PI3-kinase (show PIK3CA Proteins)/Akt (show AKT1 Proteins) signaling pathway
Caspase-3 (show CASP3 Proteins) is a stress intensity sensor that controls cell fate by either initiating a RasGAP cleavage-dependent cell resistance program or a cell suicide response mediated by akt (show AKT1 Proteins).
The protein encoded by this gene is located in the cytoplasm and is part of the GAP1 family of GTPase-activating proteins. The gene product stimulates the GTPase activity of normal RAS p21 but not its oncogenic counterpart. Acting as a suppressor of RAS function, the protein enhances the weak intrinsic GTPase activity of RAS proteins resulting in the inactive GDP-bound form of RAS, thereby allowing control of cellular proliferation and differentiation. Mutations leading to changes in the binding sites of either protein are associated with basal cell carcinomas. Mutations also have been associated with hereditary capillary malformations (CM) with or without arteriovenous malformations (AVM) and Parkes Weber syndrome. Alternative splicing results in two isoforms where the shorter isoform, lacking the N-terminal hydrophobic region but retaining the same activity, appears to be abundantly expressed in placental but not adult tissues.
, Ras GTPase-activating protein
, vacuolar peduncule
, vacuolar pedunculi
, ras GTPase-activating protein 1
, triphosphatase-activating protein
, GTPase-activating protein
, RAS p21 protein activator (GTPase activating protein RAS p21)
, RAS p21 protein activator 1