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Study shows that USP9X (show USP9X Proteins) deubiquitylating enzyme maintains RAPTOR protein levels, mTORC1 signalling and proliferation in neural progenitors. USP9X (show USP9X Proteins) is the first deubiquitylating enzyme shown to stabilize RAPTOR.
Results suggest that RPTOR mediates, at least partially, the resistance to EGFR (show EGFR Proteins) inhibition in triple-negative breast cancer cells.
data reveal that RAPTOR up-regulation contributes to PI3K (show PIK3CA Proteins)-mTOR (show FRAP1 Proteins) inhibitor resistance, and suggest that RAPTOR expression should be included in the pharmacodynamic assessment of mTOR (show FRAP1 Proteins) kinase inhibitor trials
Hypomethylation of CpG sites in RPTOR, MGRN1 (show MGRN1 Proteins) and RAPSN (show RAPSN Proteins) in blood is associated with breast cancer.
RPTOR (regulatory associated protein of mTOR, complex 1) is a novel target of miR (show MLXIP Proteins)-155 in CF lung epithelial cells. The suppression of RPTOR expression and subsequent activation of TGF-beta (show TGFB1 Proteins) signaling resulted in the induction of fibrosis by elevating connective tissue growth factor (CTGF (show CTGF Proteins)) abundance in CF lung epithelial cells.
Data show that mTOR (show FRAP1 Proteins) protein forms a complex with Raptor and estrogen receptor-alpha (ERalpha (show ESR1 Proteins)).
Up-regulation of mTORC1 via raptor by aldosterone is a critical pathobiologic mechanism that controls pulmonary artery smooth muscle cell survival to promote hypertrophic vascular remodeling and pulmonary arterial hypertension.
Hgh mTOR (show FRAP1 Proteins) 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.
revealed more than 170 NFAT-associated proteins, half of which are involved in transcriptional regulation. Among them are many hitherto unknown interaction partners of NFATc1 and NFATc2 in T cells, such as Raptor, CHEK1, CREB1, RUNX1, SATB1, Ikaros, and Helios.
In this study we began by validating the expression of four main mTOR (show FRAP1 Proteins) pathway components, mTOR (show FRAP1 Proteins), DEPTOR (show DEPTOR Proteins), rictor and raptor, at gene and protein level in in vitro models of endometrioid (MDAH2774) and clear cell (SKOV3) ovarian cancer
Our study provides, for the first time, a global analysis of phosphorylation events in spermatogonial progenitor cells (SPCs) in response to GDNF, and we have identified activation of mTORC1 signaling through ERK kinase-mediated phosphorylation of multiple sites of raptor protein as an important pathway for SPC proliferation.
Thus, the various regulatory elements that impinge upstream of mTORC1 activation pathways are differentially required for HSC (show FUT1 Proteins) homeostasis in vivo.
Deletion of Raptor reduced the size of limb bud cells, resulting in overall diminution of the limb bud without affecting skeletal patterning. We then examined the potential role of mTORC1 in chondrogenic differentiation in vitro.
Results provide genetic evidence indicating that mTOR (show FRAP1 Proteins) 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 (show FRAP1 Proteins) signaling to modulate Stat3 (show STAT3 Proteins) activity and further promotes axon regeneration.
This study demonstrated that Loss of the Rptor gene in mice neural progenitor cells affects normal development in young age and may contribute to alleviate KA seizure-induced behavioral abnormalities, suggesting that raptor protein plays an important role in seizure comorbidities.
These results demonstrate that mTORC1 has an essential role in the meiotic progression and silencing of sex chromosomes in the male germline, based on conditional knockdown of its core component, Raptor.
Rptor/mTORC1 signalling supports germinal center B cell responses at both early and late GC phases during viral infection but does not regulate GCB (show NPR2 Proteins) cell differentiation into memory B cells and plasma cells at the late GC stage.
mitochondrial dysfunction triggers LKB1 (show STK11 Proteins)-mediated AMPK (show PRKAA1 Proteins) activation, which stimulates Sirt2 (show SIRT2 Proteins) phosphorylation, leading to activation of mTOR (show FRAP1 Proteins)-RAPTOR and Glut1 (show SLC2A1 Proteins)-mediated glucose uptake.
inhibiting regulatory-associated protein of mechanistic target of rapamycin (show FRAP1 Proteins) (RPTOR) in hyperoxia settings, limited lung injury by increased autophagy, decreased apoptosis, improved lung architecture, and increased survival.
This gene encodes a component of a signaling pathway that regulates cell growth in response to nutrient and insulin levels. The encoded protein forms a stoichiometric complex with the mTOR kinase, and also associates with eukaryotic initiation factor 4E-binding protein-1 and ribosomal protein S6 kinase. The protein positively regulates the downstream effector ribosomal protein S6 kinase, and negatively regulates the mTOR kinase. Multiple transcript variants encoding different isoforms have been found for this gene.
p150 target of rapamycin (TOR)-scaffold protein containing WD-repeats
, regulatory-associated protein of mTOR
, p150 target of rapamycin (TOR)-scaffold protein