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The protein encoded by RASA1 is located in the cytoplasm and is part of the GAP1 family of GTPase-activating proteins. Zusätzlich bieten wir Ihnen RASA1 Kits (14) und RASA1 Proteine (4) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 97 products:
Human Polyclonal RASA1 Primary Antibody für EIA, WB - ABIN954457
Hemerly, Bastos, Cerutti: Identification of several novel non-p.R132 IDH1 variants in thyroid carcinomas. in European journal of endocrinology / European Federation of Endocrine Societies 2010
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Human Monoclonal RASA1 Primary Antibody für WB - ABIN395417
Wiemels, Kang, Chang, Zheng, Kouyoumji, Zhang, Smith, Scelo, Metayer, Buffler, Wiencke: Backtracking RAS mutations in high hyperdiploid childhood acute lymphoblastic leukemia. in Blood cells, molecules & diseases 2010
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Human Polyclonal RASA1 Primary Antibody für WB - ABIN656874
Oinuma, Ito, Katoh, Negishi: Semaphorin 4D/Plexin-B1 stimulates PTEN activity through R-Ras GTPase-activating protein activity, inducing growth cone collapse in hippocampal neurons. in The Journal of biological chemistry 2010
Cow (Bovine) Monoclonal RASA1 Primary Antibody für ICC, IF - ABIN266005
Muto, Yi, Harrison, Dávalos, Fancher, Ziegler, Feigel, Kondo, Nishibe, Sessa, Dardik: Eph-B4 prevents venous adaptive remodeling in the adult arterial environment. in The Journal of experimental medicine 2011
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 (zeige PTPN1 Antikörper) dephosphorylates PITX1 (zeige PITX1 Antikörper) to weaken its protein stability and the transcriptional activity for p120RasGAP gene expression
Data suggest that, in response to netrin-1 (zeige NTN1 Antikörper)/netrin receptor (DCC (zeige DCC Antikörper)) signaling, p120RasGAP is recruited to growth cones and supports axon outgrowth; p120RasGAP Src (zeige SRC Antikörper) 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.
This is the second largest study on isolated, non-syndromic Port-wine stain; data suggest that GNAQ (zeige GNAQ Antikörper) is the main genetic determinant in this condition. Moreover, isolated port-wine stains are distinct from capillary malformations seen in RASA1 disorders.
Data showed that hypoxia regulated the expression of miR (zeige MLXIP Antikörper)-182 and RASA1 to promote HCC (zeige FAM126A Antikörper) angiogenesis.
p120RasGAP shields Akt (zeige AKT1 Antikörper) from deactivating phosphatases in FGF1 (zeige FGF1 Antikörper) signaling, but loses this ability once cleaved by caspase-3 (zeige CASP3 Antikörper).
Capillary malformation-arteriovenous malformation syndrome (CM-AVM) is an autosomal dominant disorder caused by RASA1 mutations.
Multifocal, small, round-to-oval, pinkish-to-red cutaneous capillary malformations are seen in more than 90% of people with RASA1 mutations.
miR-21 promotes malignant behaviors of colon cancer cells by regulating RASA1 expression via RAS pathways.
The data suggest that nitrosylation of H-Ras (zeige HRAS Antikörper) rearranges the adsorptive potential and intrinsic GTPase (zeige RACGAP1 Antikörper) activity of H-Ras (zeige HRAS Antikörper) through modification of C-terminal cysteines of molecule.
Double-deficient RASA1-neurofibromin 1 (zeige NF1 Antikörper) 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 (zeige NOTCH1 Antikörper) gene.
Rasa1 may have a role in pathogenesis of capillary malformation-arteriovenous malformation in a mouse model
Regulation of Rasa1 translation by miR (zeige MLXIP Antikörper)-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 (zeige D4S234E Antikörper) GTPase activating protein 1 (RASA1)
14-3-3 (zeige YWHAQ Antikörper) negatively regulates the RGC downstream of the PI3-kinase (zeige PIK3CA Antikörper)/Akt (zeige AKT1 Antikörper) signaling pathway
Caspase-3 (zeige CASP3 Antikörper) 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 (zeige AKT1 Antikörper).
Data reveal a role for RASA1 as a physiological negative regulator of lymphatic endothelial cell growth that maintains the lymphatic vasculature in a quiescent functional state through its ability to inhibit Ras signal transduction.
Ca2 (zeige CA2 Antikörper)+-dependent monomer and dimer formation switches CAPRI (zeige RASA4 Antikörper) Protein between Ras GTPase-activating protein (GAP) and RapGAP (zeige RAP1GAP Antikörper) activities
statins inhibit GGPP biosynthesis in the mevalonate pathway, and then inhibit signal transduction in the Ras/ERK (zeige EPHB2 Antikörper) and Ras/Akt (zeige AKT1 Antikörper) pathways, thereby inhibiting bFGF (zeige FGF2 Antikörper), HGF (zeige HGF Antikörper), TGF-beta (zeige TGFB1 Antikörper) expression
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