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抗Human RICTOR 抗体:
抗Mouse (Murine) RICTOR 抗体:
抗Rat (Rattus) RICTOR 抗体:
Human Polyclonal RICTOR Primary Antibody for IP, WB - ABIN152042
Hresko, Mueckler: mTOR.RICTOR is the Ser473 kinase for Akt/protein kinase B in 3T3-L1 adipocytes. in The Journal of biological chemistry 2005
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Human Polyclonal RICTOR Primary Antibody for FACS, ICC - ABIN152043
Jindra, Jin, Rozengurt, Reed: HLA class I antibody-mediated endothelial cell proliferation via the mTOR pathway. in Journal of immunology (Baltimore, Md. : 1950) 2008
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Human Monoclonal RICTOR Primary Antibody for IHC (p), IP - ABIN566975
Naïmi, Gautier, Chaussade, Valverde, Accili, Van Obberghen: Nuclear forkhead box O1 controls and integrates key signaling pathways in hepatocytes. in Endocrinology 2007
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Human Polyclonal RICTOR Primary Antibody for IHC (p), ELISA - ABIN543015
Jacinto, Facchinetti, Liu, Soto, Wei, Jung, Huang, Qin, Su: SIN1/MIP1 maintains rictor-mTOR complex integrity and regulates Akt phosphorylation and substrate specificity. in Cell 2006
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Human Polyclonal RICTOR Primary Antibody for IHC (p), ELISA - ABIN543016
Yang, Inoki, Ikenoue, Guan: Identification of Sin1 as an essential TORC2 component required for complex formation and kinase activity. in Genes & development 2006
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Human Monoclonal RICTOR Primary Antibody for ELISA, WB - ABIN966967
Martin, Masri, Bernath, Nishimura, Gera: Hsp70 associates with Rictor and is required for mTORC2 formation and activity. in Biochemical and biophysical research communications 2008
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Human Polyclonal RICTOR Primary Antibody for ELISA, ICC - ABIN4350526
Verreault, Weppler, Stegeman, Warburton, Strutt, Masin, Bally: Combined RNAi-mediated suppression of Rictor and EGFR resulted in complete tumor regression in an orthotopic glioblastoma tumor model. in PLoS ONE 2013
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Human Monoclonal RICTOR Primary Antibody for ELISA, FACS - ABIN4350528
Loganathan, Kandala, Gupta, Srivastava: Inhibition of EGFR-AKT axis results in the suppression of ovarian tumors in vitro and in preclinical mouse model. in PLoS ONE 2012
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mTORC2/RICTOR inhibition in melanoma cells has the potential to reduce liver metastasis in vivo via effects on tumor cell motility. mTORC2/RICTOR inhibition in melanoma cells significantly decreases the responsiveness of melanoma cells to HSC- and HGF-induced stimulation.
Rictor striatal levels could counteract neuronal dysfunction induced by mutant huntingtin.
High Rictor expression is associated with gastric cancer.
Down-regulation of miR-142-3p inhibited ECs apoptosis and atherosclerotic development by up-regulating the expression of Rictor and activating the Akt/eNOS signaling pathway.
Rictor regulates the vasculogenic mimicry of melanoma and determines the patients' survival via the AKT-MMP2-MMP9 pathway.
Autophagy regulates c-MET phosphorylation via an mTORC2-dependent mechanism.
Tumor-suppressive microRNA-218 inhibits tumor angiogenesis through RICTOR/VEGFA axis in prostate tumor cells.
Results find RICTOR frequently amplified in small cell lung cancer (SCLC) tumors and associated with decreased survival.
Study examined mTOR variables, with attention to mTORC2 (Rictor), in Alzheimer's disease (AD) brain samples and in two mouse models, and made comparisons with results from cell- and in vitro-based experiments where Abeta is either expressed or peptide added. Authors conclude that striking a new balance by restoring mTORC2 abundance and/or inhibition of mTORC1 has therapeutic potential in AD.
Missense mutation in RICTOR gene is associated with Tourette syndrome.
RICTOR amplification is a rare but therapeutically relevant genomic alteration across solid tumors. Our results support further pre-clinical and clinical investigation with AZD2014 in RICTOR amplified gastric cancer and highlights the importance of genomic profiling
miR-153 downregulation could be one important reason of Rictor upregulation and mTORC2 over-activation in glioma cells. Further, miR-153-induced anti-glioma cell activity is possibly via downregulating Rictor.
These results point to an increase in total and phosphorylated Akt in high-grade gliomas and to a possible role of RICTOR in proliferations of high-grade glioblastomas cells.
Hgh mTOR activity and Rictor overexpression could be markers of a bad prognosis. Combined phosphoprotein and Rictor/Raptor expression evaluation revealed even stronger statistical correlation with prognosis.
In this study we began by validating the expression of four main mTOR pathway components, mTOR, DEPTOR, rictor and raptor, at gene and protein level in in vitro models of endometrioid (MDAH2774) and clear cell (SKOV3) ovarian cancer
Based on univariate and multivariate Cox proportional hazards regression analysis, RICTOR-positive expression, AJCC staging III or IV and nodal metastasis are prognostic factors and the former two are independent risk factors for esophageal squamous cell carcinoma.
Taken together, our results suggest that the proinflammatory cytokine TNFalpha promotes the expression of Rictor through the NF-kappaB pathway in renal cell carcinoma.
RICTOR amplification may define a novel and unique molecular subset of patients with lung cancer who may benefit from treatment with mTORC1/2 inhibitors.
Data show that rapamycin-insensitive companion of mTOR protein (RICTOR) plays a central role in phosphatidylinositol 3-kinase (PI3K)/proto-oncogene protein c-akt (AKT) pathway in melanocytes and its deregulation could be involved in melanoma development.
Mdm20 acts as a novel regulator of Rictor, thereby controlling mTORC2 activity, and leading to the activation of PKCalphaS657 and FoxO1.
It has been shown, via conditional deletion of Raptor (mTORC1) or Rictor (mTORC2), that mTORC1 and mTORC2 promote NK cell maturation in a cooperative and non-redundant manner, mainly by controlling the expression of Tbx21 and Eomes.
Data provides evidence that rictor protein binds to hnrnp protein.
Rictor deficiency increases macrophage/neutrophil infiltration and cytokine/chemokine release during hepatic Ischemia/Reperfusion injury. In addition, Rictor deficiency affected MAPK activation in lipopolysaccharide -treated RAW264.7 cells.
Rictor-deficient keratinocytes exhibited changes in global gene expression profiles consistent with metabolic alterations and enhanced stress tolerance, a shift in cell catabolic processes from glycids and lipids to glutamine consumption and increased production of mitochondrial reactive oxygen species.
Osteoblast differentiation was reduced, with down-regulation of mTORC2 signaling activity in primary cultures of osteoblasts that did not contain rictor.
To determine the role of mTORC2 signaling in myelinogenesis, we generated a mouse lacking the critical mTORC2 component Rictor in oligodendrocyte precursors (OPCs). Targeted deletion of Rictor in these cells decreases and delays the expression of myelin related proteins and reduces the size of cerebral white matter tracts
results demonstrated that Rictor/mTORC2 might play an important role in the cardiomyocyte differentiation of mES cells.
Results provide genetic evidence indicating that mTOR and Raptor are required for sensory axon regeneration enhanced by peripheral lesions in mice, whereas Rictor plays a minor role. The peripheral lesion activates rapamycin-resistant mTOR signaling to modulate Stat3 activity and further promotes axon regeneration.
Increased oxidative stress leads to oxidation of mTORC2 complex protein Rictor.
Rictor positively regulates B cell receptor (BCR) signaling via up-regulating Btk and down-regulating SH2-containing inositol phosphatase. Rictor regulates BCR signaling via actin reorganization.
our present findings highlighted a pivotal regulatory axis of Rictor-FoxO3a in maintaining quiescence and the stemness of LSCs.
These findings reveal a novel functional pathway important for age-related bone loss and support for miR-218 and Rictor as potential targets for therapeutic intervention for age-related osteoporosis treatment.
this study shows that Rictor is required for NKT-17 cell development and normal iNKT-cell cytolytic function
data suggest that Rictor/mTORC2 controls an amino acid-sensitive checkpoint that allows T cells to determine whether the microenvironment contains sufficient resources for daughter cell generation.
Loss of DNMT3B results in hypomethylation of the miR-196b promoter and increased miR-196b expression, which directly targets the mTORC2 component Rictor.
Rictor in the limb mesenchymal lineage is required for the normal response to the anti-sclerostin therapy in both bone formation and resorption.
Low RICTOR expression was detected in quiescent, confluent mouse aortic endothelial cells, whereas high doses of FGF2 induced high RICTOR expression that was associated with strong mTORC2-specific protein kinase Ca and AKT phosphorylation
RICTOR and MTOR (FRAP1\; MIM 601231) are components of a protein complex that integrates nutrient- and growth factor-derived signals to regulate cell growth (Sarbassov et al., 2004
rapamycin-insensitive companion of mTOR
, AVO3 homolog
, TORC2-specific protein AVO3
, protein pianissimo
, FYN binding protein
, rapamycin insensitive companion of mTOR