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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 ELISA Kits)-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 ELISA Kits), Bad, or Survivin (show BIRC5 ELISA Kits) are not required for p120 RasGAP fragment N to protect cells from cell death; conclude that downstream targets of Akt (show AKT1 ELISA Kits) other than mTORC1, Bad, or survivin (show BIRC5 ELISA Kits) mediate fragment N-induced protection or that several Akt (show AKT1 ELISA Kits) effectors can compensate for each other to induce the pro-survival fragment N-dependent responses
The interaction between RASA1 and EPHB4 (show EPHB4 ELISA Kits) 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 ELISA Kits) stabilized RASA1 mRNA via directly binding to the QKI (show QKI ELISA Kits) response element region of RASA1, which in turn prevented the activation of the Ras-MAPK (show MAPK1 ELISA Kits) 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 ELISA Kits) dephosphorylates PITX1 (show PITX1 ELISA Kits) to weaken its protein stability and the transcriptional activity for p120RasGAP gene expression
Data suggest that, in response to netrin-1 (show NTN1 ELISA Kits)/netrin receptor (DCC (show DCC ELISA Kits)) signaling, p120RasGAP is recruited to growth cones and supports axon outgrowth; p120RasGAP Src (show SRC ELISA Kits) homology 2 domains exhibit scaffolding properties sufficient to support axon outgrowth.
The data suggest that nitrosylation of H-Ras (show HRAS ELISA Kits) rearranges the adsorptive potential and intrinsic GTPase (show RACGAP1 ELISA Kits) activity of H-Ras (show HRAS ELISA Kits) 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 ELISA Kits)/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 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits)-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 ELISA Kits) negatively regulates the RGC downstream of the PI3-kinase (show PIK3CA ELISA Kits)/Akt (show AKT1 ELISA Kits) signaling pathway
Caspase-3 (show CASP3 ELISA Kits) 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 ELISA Kits).
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