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anti-Human RASA1 Anticorps:
anti-Rat (Rattus) RASA1 Anticorps:
anti-Mouse (Murine) RASA1 Anticorps:
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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.
RASA1 variants are rarely found in children with sporadic capillary malformations of lower limbs without capillary malformation-arteriovenous malformation syndrome.
we demonstrated a novel oncogenic mechanism of PTP1B (Montrer PTPN1 Anticorps) on affecting PITX1 (Montrer PITX1 Anticorps)/p120RasGAP in colorectal carcinoma(CRC (Montrer CALR Anticorps)). Regorafenib inhibited CRC (Montrer CALR Anticorps) survival through reserving PTP1B (Montrer PTPN1 Anticorps)-dependant PITX1 (Montrer PITX1 Anticorps)/p120RasGAP downregulation. PTP1B (Montrer PTPN1 Anticorps) may be a potential biomarker predicting regorafenib effectiveness, and a potential solution for CRC (Montrer CALR Anticorps)
RASA1 mutations are associated melanoma tumorigenesis.
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 (Montrer MLXIP Anticorps)-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 (Montrer FRAP1 Anticorps), Bad, or Survivin are not required for p120 RasGAP fragment N to protect cells from cell death; conclude that downstream targets of Akt (Montrer AKT1 Anticorps) other than mTORC1, Bad, or survivin mediate fragment N-induced protection or that several Akt (Montrer AKT1 Anticorps) effectors can compensate for each other to induce the pro-survival fragment N-dependent responses
The interaction between RASA1 and EPHB4 (Montrer EPHB4 Anticorps) 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 Anticorps) stabilized RASA1 mRNA via directly binding to the QKI (Montrer QKI Anticorps) response element region of RASA1, which in turn prevented the activation of the Ras-MAPK (Montrer MAPK1 Anticorps) signaling pathway, suppressed cellular proliferation and induced cell cycle arrest.
The data suggest that nitrosylation of H-Ras (Montrer HRAS Anticorps) rearranges the adsorptive potential and intrinsic GTPase (Montrer RACGAP1 Anticorps) activity of H-Ras (Montrer HRAS Anticorps) 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 Anticorps)/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 Anticorps) 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 Anticorps) 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 Anticorps)-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 (Montrer D4S234E Anticorps) GTPase activating protein 1 (RASA1)
14-3-3 (Montrer YWHAQ Anticorps) negatively regulates the RGC downstream of the PI3-kinase (Montrer PIK3CA Anticorps)/Akt (Montrer AKT1 Anticorps) signaling pathway
Caspase-3 (Montrer CASP3 Anticorps) 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 Anticorps).
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