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Study found that nuclear expression of raptor in luminal A-like breast tumors predicted a group of patients with good prognosis but with no clear benefit of tamoxifen treatment. Additionally, study found co-localization of raptor and estrogen receptor-alpha (ERalpha) upon estrogen stimulation in ERalpha-positive, but not in ERalpha-negative breast cancer cells.
Study shows that USP9X deubiquitylating enzyme maintains RAPTOR protein levels, mTORC1 signalling and proliferation in neural progenitors. USP9X is the first deubiquitylating enzyme shown to stabilize RAPTOR.
Results suggest that RPTOR mediates, at least partially, the resistance to EGFR inhibition in triple-negative breast cancer cells.
data reveal that RAPTOR up-regulation contributes to PI3K-mTOR inhibitor resistance, and suggest that RAPTOR expression should be included in the pharmacodynamic assessment of mTOR kinase inhibitor trials
Hypomethylation of CpG sites in RPTOR, MGRN1 and RAPSN in blood is associated with breast cancer.
RPTOR (regulatory associated protein of mTOR, complex 1) is a novel target of miR-155 in CF lung epithelial cells. The suppression of RPTOR expression and subsequent activation of TGF-beta signaling resulted in the induction of fibrosis by elevating connective tissue growth factor (CTGF) abundance in CF lung epithelial cells.
Data show that mTOR protein forms a complex with Raptor and estrogen receptor-alpha (ERalpha).
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 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 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
Our results demonstrate for the first time that the expression quantitative trait loci of RPTOR, rs7502563, is susceptible to glioma
The positive regulation of mTORC1 activity by NPRL2 is mediated through NPRL2 interaction with Raptor.
Propose regulation of placental SNAT2/LAT1 ubiquitination by mTORC1 and Nedd4-2.
RPTOR was not associated with bipolar disorder or schizophrenia.
microRNA-210 and raptor are involved in mithramycin-mediated erythroid differentiation of K562 cells and participate to the fine-tuning and control of gamma-globin gene expression in erythroid precursor cells.
the expressions of Beclin1, Raptor, and Rictor are related to the development and progression of colorectal carcinoma and multidrug resistance.
Common genetic variation in RPTOR is associated with overweight/obesity but does not discernibly contribute to either essential hypertension or isolated systolic hypertension in the Hawaiian population studied.
Studied the impact of SNPs in/near UCP3 and RPTOR on obesity-related traits.
phosphorylating the T-loop Akt residue Thr(308) by PDK1 requires Raptor of the mTORC1 complex as a platform or scaffold protein.
Study reveals that enterocyte specific Raptor is required for initiating a type 2 immune response which appears to function through the regulation of mTORC1 activity.
Raptor-deficient beta cells display reduced glucose responsiveness and exhibit a glucose metabolic profile resembling fetal beta cells.
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.
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 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 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.
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 cell differentiation into memory B cells and plasma cells at the late GC stage.
mitochondrial dysfunction triggers LKB1-mediated AMPK activation, which stimulates Sirt2 phosphorylation, leading to activation of mTOR-RAPTOR and Glut1-mediated glucose uptake.
inhibiting regulatory-associated protein of mechanistic target of rapamycin (RPTOR) in hyperoxia settings, limited lung injury by increased autophagy, decreased apoptosis, improved lung architecture, and increased survival.
Loss of Raptorin in osteoclasts led to an increase in bone mass with decreased bone resorption.
Raptor knockout mice are lean and insulin resistant with increased energy expenditure, and they are resistant to a high-fat diet.
The findings reveal HDAC5-mTORC1 signaling as a novel mechanism in the differential regulation of gastric ghrelin and nesfatin-1.
critical roles in thymopoiesis and thymus function
data suggest that EtOH-induced decreases in protein synthesis in fasted mice may be independent of mTORC1 and MAPK signaling.
Raptor negatively regulates hepatic Akt activity and lipogenesis via PHLPP2 stabilization.
mTOR kinase-dependent, but raptor-independent regulation of downstream signaling is important for myogenic differentiation.
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