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miR (show MLXIP ELISA Kits)-153 downregulation could be one important reason of Rictor upregulation and mTORC2 (show CRTC2 ELISA Kits) over-activation in glioma cells. Further, miR (show MLXIP ELISA Kits)-153-induced anti-glioma cell activity is possibly via downregulating Rictor.
These results point to an increase in total and phosphorylated Akt (show AKT1 ELISA Kits) in high-grade gliomas and to a possible role of RICTOR in proliferations of high-grade glioblastomas cells.
Hgh mTOR (show FRAP1 ELISA Kits) activity and Rictor overexpression could be markers of a bad prognosis. Combined phosphoprotein and Rictor/Raptor (show RPTOR ELISA Kits) expression evaluation revealed even stronger statistical correlation with prognosis.
In this study we began by validating the expression of four main mTOR (show FRAP1 ELISA Kits) pathway components, mTOR (show FRAP1 ELISA Kits), DEPTOR (show DEPTOR ELISA Kits), rictor and raptor (show RPTOR ELISA Kits), at gene and protein level in in vitro models of endometrioid (MDAH2774) and clear cell (SKOV3) ovarian cancer
Based on univariate and multivariate Cox (show COX8A ELISA Kits) 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 (show PIK3CA ELISA Kits))/proto-oncogene (show RAB1A ELISA Kits) protein c (show PROC ELISA Kits)-akt (AKT (show AKT1 ELISA Kits)) pathway in melanocytes and its deregulation could be involved in melanoma development.
Mdm20 (show NAA25 ELISA Kits) acts as a novel regulator of Rictor, thereby controlling mTORC2 (show CRTC2 ELISA Kits) activity, and leading to the activation of PKCalphaS657 and FoxO1 (show FOXO1 ELISA Kits).
RICTOR/MTORC2 (show CRTC2 ELISA Kits)-AKT (show AKT1 ELISA Kits) can integrate convergent hormonal and metabolic signals to provide coordinated and sensitive regulation of hepatic FOXO1 (show FOXO1 ELISA Kits)-target gene expression.
results demonstrated that Rictor/mTORC2 (show CRTC2 ELISA Kits) might play an important role in the cardiomyocyte differentiation of mES (show PTCH1 ELISA Kits) cells.
Results provide genetic evidence indicating that mTOR (show FRAP1 ELISA Kits) and Raptor (show RPTOR ELISA Kits) 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 (show FRAP1 ELISA Kits) signaling to modulate Stat3 (show STAT3 ELISA Kits) activity and further promotes axon regeneration.
Increased oxidative stress leads to oxidation of mTORC2 (show CRTC2 ELISA Kits) 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 (show FOXO3 ELISA Kits) 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 (show MLXIP ELISA Kits)-218 and Rictor as potential targets for therapeutic intervention for age-related osteoporosis treatment.
this study shows that Rictor is required for NKT (show CTSL1 ELISA Kits)-17 cell development and normal iNKT-cell cytolytic function
data suggest that Rictor/mTORC2 (show CRTC2 ELISA Kits) 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 (show DNMT3B ELISA Kits) results in hypomethylation of the miR (show MLXIP ELISA Kits)-196b promoter and increased miR (show MLXIP ELISA Kits)-196b expression, which directly targets the mTORC2 (show CRTC2 ELISA Kits) component Rictor.
Rictor in the limb mesenchymal lineage is required for the normal response to the anti-sclerostin (show SOST ELISA Kits) therapy in both bone formation and resorption.
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