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We found that neither S6K-dependent cell growth nor S6K-Thr-398 phosphorylation was affected in rictor-null mutants.
Study shows that USP9X (Montrer USP9X Protéines) deubiquitylating enzyme maintains RAPTOR protein levels, mTORC1 signalling and proliferation in neural progenitors. USP9X (Montrer USP9X Protéines) is the first deubiquitylating enzyme shown to stabilize RAPTOR.
Results suggest that RPTOR mediates, at least partially, the resistance to EGFR (Montrer EGFR Protéines) inhibition in triple-negative breast cancer cells.
data reveal that RAPTOR up-regulation contributes to PI3K (Montrer PIK3CA Protéines)-mTOR (Montrer FRAP1 Protéines) inhibitor resistance, and suggest that RAPTOR expression should be included in the pharmacodynamic assessment of mTOR (Montrer FRAP1 Protéines) kinase inhibitor trials
Hypomethylation of CpG sites in RPTOR, MGRN1 (Montrer MGRN1 Protéines) and RAPSN (Montrer RAPSN Protéines) in blood is associated with breast cancer.
RPTOR (regulatory associated protein of mTOR, complex 1) is a novel target of miR (Montrer MLXIP Protéines)-155 in CF lung epithelial cells. The suppression of RPTOR expression and subsequent activation of TGF-beta (Montrer TGFB1 Protéines) signaling resulted in the induction of fibrosis by elevating connective tissue growth factor (CTGF (Montrer CTGF Protéines)) abundance in CF lung epithelial cells.
Data show that mTOR (Montrer FRAP1 Protéines) protein forms a complex with Raptor and estrogen receptor-alpha (ERalpha (Montrer ESR1 Protéines)).
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 (Montrer FRAP1 Protéines) 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 (Montrer NFATC1 Protéines)-associated proteins, half of which are involved in transcriptional regulation. Among them are many hitherto unknown interaction partners of NFATc1 (Montrer NFATC1 Protéines) and NFATc2 (Montrer NFAT1 Protéines) in T cells, such as Raptor, CHEK1 (Montrer CHEK1 Protéines), CREB1 (Montrer CREB1 Protéines), RUNX1 (Montrer RUNX1 Protéines), SATB1 (Montrer SATB1 Protéines), Ikaros (Montrer IKZF1 Protéines), and Helios (Montrer ZNFN1A2 Protéines).
In this study we began by validating the expression of four main mTOR (Montrer FRAP1 Protéines) pathway components, mTOR (Montrer FRAP1 Protéines), DEPTOR (Montrer DEPTOR Protéines), 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 (Montrer FUT1 Protéines) 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 (Montrer FRAP1 Protéines) 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 (Montrer FRAP1 Protéines) signaling to modulate Stat3 (Montrer STAT3 Protéines) 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 (Montrer NPR2 Protéines) cell differentiation into memory B cells and plasma cells at the late GC stage.
mitochondrial dysfunction triggers LKB1 (Montrer STK11 Protéines)-mediated AMPK (Montrer PRKAA1 Protéines) activation, which stimulates Sirt2 (Montrer SIRT2 Protéines) phosphorylation, leading to activation of mTOR (Montrer FRAP1 Protéines)-RAPTOR and Glut1 (Montrer SLC2A1 Protéines)-mediated glucose uptake.
inhibiting regulatory-associated protein of mechanistic target of rapamycin (Montrer FRAP1 Protéines) (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.
, target of rapamycin (TOR)-associated protein
, Raptor family protein
, WD40 repeat-containing protein
, armadillo-like helical domain-containing protein
, p150 target of rapamycin (TOR)-scaffold protein containing WD-repeats
, regulatory-associated protein of mTOR
, p150 target of rapamycin (TOR)-scaffold protein