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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 (zeige MLXIP ELISA Kits)-153 downregulation could be one important reason of Rictor upregulation and mTORC2 (zeige CRTC2 ELISA Kits) over-activation in glioma cells. Further, miR (zeige 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 (zeige AKT1 ELISA Kits) in high-grade gliomas and to a possible role of RICTOR in proliferations of high-grade glioblastomas cells.
Hgh mTOR (zeige FRAP1 ELISA Kits) activity and Rictor overexpression could be markers of a bad prognosis. Combined phosphoprotein and Rictor/Raptor (zeige 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 (zeige FRAP1 ELISA Kits) pathway components, mTOR (zeige FRAP1 ELISA Kits), DEPTOR (zeige DEPTOR ELISA Kits), rictor and raptor (zeige 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 (zeige 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 (zeige PIK3CA ELISA Kits))/proto-oncogene (zeige RAB1A ELISA Kits) protein c (zeige PROC ELISA Kits)-akt (AKT (zeige AKT1 ELISA Kits)) pathway in melanocytes and its deregulation could be involved in melanoma development.
Mdm20 (zeige NAA25 ELISA Kits) acts as a novel regulator of Rictor, thereby controlling mTORC2 (zeige CRTC2 ELISA Kits) activity, and leading to the activation of PKCalphaS657 and FoxO1 (zeige FOXO1 ELISA Kits).
Osteoblast differentiation was reduced, with down-regulation of mTORC2 (zeige CRTC2 ELISA Kits) signaling activity in primary cultures of osteoblasts that did not contain rictor.
To determine the role of mTORC2 (zeige CRTC2 ELISA Kits) signaling in myelinogenesis, we generated a mouse lacking the critical mTORC2 (zeige CRTC2 ELISA Kits) 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 (zeige CRTC2 ELISA Kits) might play an important role in the cardiomyocyte differentiation of mES (zeige PTCH1 ELISA Kits) cells.
Results provide genetic evidence indicating that mTOR (zeige FRAP1 ELISA Kits) and Raptor (zeige 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 (zeige FRAP1 ELISA Kits) signaling to modulate Stat3 (zeige STAT3 ELISA Kits) activity and further promotes axon regeneration.
Increased oxidative stress leads to oxidation of mTORC2 (zeige 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 (zeige 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 (zeige 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 (zeige CTSL1 ELISA Kits)-17 cell development and normal iNKT-cell cytolytic function
data suggest that Rictor/mTORC2 (zeige 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.
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