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MiR (show MLXIP ELISA Kits)-137 inhibited cell proliferation and migration of vascular smooth muscle cells via targeting IGFBP-5 (show IGFBP5 ELISA Kits) and modulating the mTOR/STAT3 (show STAT3 ELISA Kits) signaling.
we describe siblings from a non-consanguineous German family in whom we identified the same heterozygous missense mutation in MTOR. in all reported families with Smith-Kingsmore syndrome and the MTOR c.5395G>A mutation, do not have detectable levels of the mutation in tested tissues, lending credence to gonadal mosaicism as the underlying mechanism
VC-A also down-regulated the expression of prosurvival phospho-AKT (p-AKT (show AKT1 ELISA Kits)), nuclear factor kappa B (NF-kB) (p65) and phospho-mammalian target of rapamycin (p-mTOR) signaling proteins.
Studies indicate that understanding mTOR network circuitry will provide insight into its deregulation in diabetes, cancer, and cardiovascular disease, but modeling in silico to elucidate how insulin (show INS ELISA Kits) activates mTORC2 (show CRTC2 ELISA Kits) remains poorly defined.
Suggest the association of activation of Akt (show AKT1 ELISA Kits)-mTOR pathway proteins and PDGFR-beta (show PDGFRB ELISA Kits) in fibrosarcomatous transformation of dermatofibrosarcoma protuberans.
These results reveal that mTOR is a new type of calmodulin-dependent kinase (show CAMK2 ELISA Kits), and TRPML1 (show MCOLN1 ELISA Kits), lysosomal calcium and calmodulin (show CALM1 ELISA Kits) play essential regulatory roles in the mTORC1 signaling pathway.
High mTOR expression is associated with gastrointestinal neuroendocrine tumors.
Rab13 (show RAB13 ELISA Kits) activated the downstream AMPK (show PRKAA1 ELISA Kits) and blocked mTOR signaling by its functional interaction with Grb2 (show GRB2 ELISA Kits) to regulate autophagy in human vascular endothelial cells.
we found that PPARdelta (show PPARD ELISA Kits) directly regulated neutral amino acid transporter (show SLC6A19 ELISA Kits) SLC1 (show MCHR1 ELISA Kits)-A5 (solute carrier family 1 member 5 (show SLC1A5 ELISA Kits)) and glucose transporter-1 (Glut1 (show SLC2A1 ELISA Kits)) gene transcription, leading to uptake of glucose and amino acid, activation of mTOR signaling, and tumor progression. In contrast, silence of PPARdelta (show PPARD ELISA Kits) or its antagonist inhibited this event.
These findings uncover ZNRF2 as a component of the amino acid sensing machinery that acts upstream of Rag-GTPases and the V-ATPase (show ATP6V1H ELISA Kits) to activate mTORC1.
High mTOR expression is associated with myeloproliferative neoplasm.
mTOR inhibition promotes growth of cells reliant on eating extracellular protein. This growth enhancement depends on mTORC1's canonical function in controlling translation rate: mTOR inhibition slows translation, thereby matching protein synthesis to the limited amino acid supply.
Data provide direct evidence for cell survival upon mTOR inhibition through mitochondrial hyperfusion employing MTFP1 as a critical effector of mTORC1 to govern cell fate decisions.
Here, the authors report the dysregulation of mTOR signaling in Pompe disease muscle cells.
Direct Sensing of TLR7 (show TLR7 ELISA Kits) Ligands and Type I IFN by the Common Myeloid Progenitor Promotes mTOR/PI3K-Dependent Emergency Myelopoiesis
p53 (show TP53 ELISA Kits)-dependent coordination with SESN2 (show SESN2 ELISA Kits) regulates AMPK (show PRKAA1 ELISA Kits) and mTORC1 signaling and controls parturition timing
mTOR signaling contributes to stem cell dysfunction and cell fate decisions in response to endogenous DNA damage
role in signaling and metabolic reprogramming for M-CSF (show CSF1R ELISA Kits)-mediated myelopoiesis
results establish a novel mechanism by which mTORC1 regulates Th1 differentiation, through control of T-bet phosphorylation
Tsc2 (show TSC2 ELISA Kits)-mTOR signaling in mesenchyme is essential for the maintenance of renal structure and for lung alveolarization.
This study reveals the dramatic rescue effects of L-leucine stimulation of mTORC1 in RBS (show ESCO2 ELISA Kits) cells and supports that normal gene expression and translation requires ESCO2 (show ESCO2 ELISA Kits) function.
By inhibiting mTOR signaling via Fbxw7 (show FBXW7 ELISA Kits), the amount of myelination during development is reduced.
Apc mutations activate mechanistic target of rapamycin complex 1 in mice and zebrafish
In our zebrafish model, autophagy induction does not depend on inhibition of the Tor pathway or activation of Tp53 (show TP53 ELISA Kits).
TOR signaling is a common pathological pathway that can be leveraged for therapeutic benefits in cardiomyopathies of different origins.
in addition to regulating cell growth and proliferation, TOR signaling controls the developmental program guiding epithelial morphogenesis in the intestine
The immunoprecipitation results also showed that high AA concentrations significantly increased the interaction of mTOR and PPARg (show PPARG ELISA Kits). In summary, PPARg (show PPARG ELISA Kits) plays an important role in the regulation of IGF-1 (show IGF1 ELISA Kits) secretion and gene expression in response to dietary protein.
These results indicate glycine enhances muscle protein mass under an inflammatory condition. The beneficial roles of glycine on the muscle are closely associated with maintaining Akt (show AKT1 ELISA Kits)-mTOR-FOXO1 (show FOXO1 ELISA Kits) signaling and suppressing the activation of TLR4 (show TLR4 ELISA Kits) and/or NOD2 (show NOD2 ELISA Kits) signaling pathways.
Data show that the amount of proteins related to mechanistic target of rapamycin (mTOR) signaling pathways decreased along crypt-villus axis (CVA).
AMPK (show PRKAA1 ELISA Kits)-mTOR-autophagy signaling is altered by intrauterine growth restriction in newborn piglets.
Uroguanylin (show GUCA2B ELISA Kits) modulates (Na++K+)ATPase (show ATP1A1 ELISA Kits) in a proximal tubule cells via cGMP/protein kinase (show CDK7 ELISA Kits) G, cAMP/protein kinase A, and mTOR pathways.
mTOR is involved in 17beta-estradiol-induced, cultured immature boar Sertoli cell proliferation via regulating the expression of SKP2, CCND1 (show CCND1 ELISA Kits), and CCNE1 (show CCNE1 ELISA Kits).
L-Glutamine enhances enterocyte growth via activation of the mTOR.
Arg, Leu, and Gln act coordinately to stimulate proliferation of pTr cells through activation of the MTOR-RPS6K-RPS6 (show RPS6 ELISA Kits)-EIF4EBP1 (show EIF4EBP1 ELISA Kits) signal transduction pathway.
Data indicate that the expression of MAP1LC3A (show MAP1LC3A ELISA Kits), B and autophagy-associated genes (ATG5 (show ATG5 ELISA Kits), mTOR, Beclin-1 (show BECN1 ELISA Kits)) was increased in normal pigs, while decreased in miniature pigs.
Biochemical, cellular, and molecular data suggest that L-arginine (show GATM ELISA Kits) stimulates mTOR biosynthesis, mTOR signaling, and overall protein biosynthesis/turnover in placental/trophoblast and blastocyst/ectoderm cells thereby enhancing cell proliferation.
These findings suggest that mTOR is involved in the control of the expression of multiple genes in cattle, which may be triggered by the luteinizing hormone surge.
14-3-3gamma (show YWHAG ELISA Kits) affects mTOR protein pathway and regulates lactogenesis in dairy cow mammary epithelial cells.
Methionine promoted casein synthesis, and this may be mediated by enhanced intracellular substrate availability and by activating JAK2 (show JAK2 ELISA Kits)-STAT5 (show STAT5A ELISA Kits) and mTOR signaling pathways.
Insulin (show INS ELISA Kits)-induced activation of phosphoinositide 3-kinase~mTOR pathway up-regulates tau protein via acceleration of protein synthesis in adrenal chromaffin cells, promoting neurite-like process outgrowth.
IGF-I (show IGF1 ELISA Kits) down-regulated functional IGF-I receptor (show IGF1R ELISA Kits) via GSK-3beta (show GSK3b ELISA Kits) inhibition and mTOR activation; constitutive activity of GSK-3beta (show GSK3b ELISA Kits) maintained IGF-I receptor (show IGF1R ELISA Kits) level in nonstimulated cells.
stimulation of mammary protein synthesis by amino acids and its enhancement by a combination of the lactogenic hormones hydrocortisone, insulin (show INS ELISA Kits), and prolactin (show PRL ELISA Kits) were associated with increased phosphorylation of the mTOR substrates
data demonstrate that hypoxia-induced adventitial fibroblast proliferation requires activation and interaction of PI3K, Akt (show AKT1 ELISA Kits), mTOR, p70S6K (show RPS6KB1 ELISA Kits), and ERK1/2 (show MAPK1/3 ELISA Kits).
prostaglandin F2alpha phosphorylates TSC2 (show TSC2 ELISA Kits) and activates mTOR and ribosomal protein S6 (show RPS6 ELISA Kits) kinase (show RPS6KB1 ELISA Kits) signaling in an AKT (show AKT1 ELISA Kits)-independent manner
mTOR links IGF-I (show IGF1 ELISA Kits) and EGF (show EGF ELISA Kits) signaling in inhibiting the autophagy pathways.
The protein encoded by this gene belongs to a family of phosphatidylinositol kinase-related kinases. These kinases mediate cellular responses to stresses such as DNA damage and nutrient deprivation. This protein acts as the target for the cell-cycle arrest and immunosuppressive effects of the FKBP12-rapamycin complex. The ANGPTL7 gene is located in an intron of this gene.
FK506 binding protein 12-rapamycin associated protein 1
, FK506 binding protein 12-rapamycin associated protein 2
, FK506-binding protein 12-rapamycin complex-associated protein 1
, FKBP-rapamycin associated protein
, FKBP12-rapamycin complex-associated protein 1
, mammalian target of rapamycin
, rapamycin and FKBP12 target 1
, rapamycin associated protein FRAP2
, rapamycin target protein 1
, serine/threonine-protein kinase mTOR
, FKBP-rapamycin associated protein (FRAP)
, FKBP-rapamycin-associated protein FRAP
, FKBP12-rapamycin complex-associated protein
, angiopoietin-like factor CDT6
, rapamycin and FKBP12 target-1 protein
, target of rapamycin