Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher toutes les espèces
Afficher tous les synonymes
Select your species
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 (Montrer FRAP1 Kits ELISA), Bad, or Survivin (Montrer BIRC5 Kits ELISA) are not required for p120 RasGAP fragment N to protect cells from cell death; conclude that downstream targets of Akt (Montrer AKT1 Kits ELISA) other than mTORC1, Bad, or survivin (Montrer BIRC5 Kits ELISA) mediate fragment N-induced protection or that several Akt (Montrer AKT1 Kits ELISA) effectors can compensate for each other to induce the pro-survival fragment N-dependent responses
The interaction between RASA1 and EPHB4 (Montrer EPHB4 Kits ELISA) 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 (Montrer QKI Kits ELISA) stabilized RASA1 mRNA via directly binding to the QKI (Montrer QKI Kits ELISA) response element region of RASA1, which in turn prevented the activation of the Ras-MAPK (Montrer MAPK1 Kits ELISA) 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 (Montrer PTPN1 Kits ELISA) dephosphorylates PITX1 (Montrer PITX1 Kits ELISA) to weaken its protein stability and the transcriptional activity for p120RasGAP gene expression
Data suggest that, in response to netrin-1 (Montrer NTN1 Kits ELISA)/netrin receptor (DCC (Montrer DCC Kits ELISA)) signaling, p120RasGAP is recruited to growth cones and supports axon outgrowth; p120RasGAP Src (Montrer SRC Kits ELISA) homology 2 domains exhibit scaffolding properties sufficient to support axon outgrowth.
Maternal and fetal capillary malformation-arteriovenous malformation due to a novel RASA1 mutation presenting with prenatal non-immune hydrops fetalis have been found.
The data suggest that nitrosylation of H-Ras (Montrer HRAS Kits ELISA) rearranges the adsorptive potential and intrinsic GTPase (Montrer RACGAP1 Kits ELISA) activity of H-Ras (Montrer HRAS Kits ELISA) 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 (Montrer CASP3 Kits ELISA)/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 (Montrer NF1 Kits ELISA) 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 (Montrer NOTCH1 Kits ELISA) gene.
Rasa1 may have a role in pathogenesis of capillary malformation-arteriovenous malformation in a mouse model
Regulation of Rasa1 translation by miR (Montrer MLXIP Kits ELISA)-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 (Montrer YWHAQ Kits ELISA) negatively regulates the RGC downstream of the PI3-kinase (Montrer PIK3CA Kits ELISA)/Akt (Montrer AKT1 Kits ELISA) signaling pathway
Caspase-3 (Montrer CASP3 Kits ELISA) 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 (Montrer AKT1 Kits ELISA).
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