Browse our anti-MTOR (FRAP1) Antibodies

Horse (Equine) Mechanistic Target of Rapamycin (serine/threonine Kinase) (FRAP1) interaction partners

1. Results indicate that adult horses may be able to increase rates of muscle protein synthesis in response to feeding and that dietary amino acids appear to be the main mediators of this effect.

Human Mechanistic Target of Rapamycin (serine/threonine Kinase) (FRAP1) interaction partners

1. mTOR mRNA and protein expression are significantly elevated in osteosarcoma tissue compared with normal control. Also, mTOR expression contributes to miR100 induced cisplatin resistance in osteosarcoma tumors.

2. 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 activates mTORC2 remains poorly defined.

3. These results define a critical role for mTOR in the regulation of the pro-inflammatory response in Fibroblast-like Synoviocyte.

4. The effects of CAPON-L overexpression on glioma cell proliferation are dependent on the AKT/mTOR/P53 activity. The overexpression of CAPON inhibits U251 cell proliferation through the AKT/mTOR signaling pathway, while overexpressing CAPON-L promoted U87 cell proliferation, possibly through down-regulating the P53 level.

5. this work revealed that SNX10 controls mTOR activation through regulating chaperone-mediated autophagy-dependent amino-acid metabolism.

6. Taken together, the present study provides the first evidence that OTUB2 acts as a pivotal driver in non-small cell lung cancer tumorigenesis by stabilizing U2AF2 and activating the AKT/mTOR pathway and the Warburg effect.

7. Both autophagy and AKT/mTOR signals were engaged in ATC cell death evoked by apatinib.

8. Mammalian Target of Rapamycin: A Metabolic Rheostat for Regulating Adipose Tissue Function and Cardiovascular Health.

9. FBW7 was decreased in renal mesangial cells induced by high glucose, and FBW7 gene overexpression can increase autophagy by inhibiting mTOR signaling and ameliorate inflammation and fibrosis.

10. Study using lung tissue and derived cultured cells from patients with chronic obstructive pulmonary disease (COPD) and from age- and sex-matched control smokers revealed that cell senescence in COPD was linked to mTOR activation, and mTOR inhibition by low-dose rapamycin prevented cell senescence and inhibited the proinflammatory senescence-associated secretory phenotype.

11. These data demonstrate a novel mTORC2-dependent apoptosis regulatory mechanism in human keratinocytes in response to UVB.

12. our results indicate that GRSF1 helps preserve mitochondrial homeostasis, in turn preventing oxidative DNA damage and the activation of mTOR and NF-kappaB, and suppressing a transcriptional pro-inflammatory program leading to increased IL6 production.

13. these data demonstrate that an oncogene-specific decoupling of mTOR from AMPK or AKT signaling accounts for alterations of resistance mechanisms and metabolic phenotypes. Indeed the inhibition of mTOR in BRAF(V600E) cells counteracts the metabolic predisposition and demonstrates mTOR as a potential target in BRAF(V600E)-driven colorectal carcinomas.

14. Long non-coding RNA DANCR contributes to lung adenocarcinoma progression by sponging miR-496 to modulate mTOR expression.

15. The LKB1/AMPK/mTOR pathway in stellate cells, and PBI-4050 may be a promising agent for treating liver fibrosis.

16. Role of Mammalian Target of Rapamycin in Atherosclerosis.

17. We here present 4 new cases of Smith-Kingsmore syndrome , review all clinical and molecular aspects of this disorder, as well as some characteristics of the patients with only brain mTOR somatic mutations.

18. The evidence has been provided for mTOR pathway activation in large vessel vasculitis.

19. This review highlights the current status of PI3K/Akt/mTOR inhibitors in B-ALL, with an emphasis on emerging evidence of the superior efficacy of synergistic combinations involving the use of traditional chemotherapeutics or other novel, targeted agents.

20. results confirm that Pulsed electromagnetic fields (PEMFs) contribute to activation of the mTOR pathway via upregulation of the proteins AKT, MAPP kinase, and RRAGA, suggesting that activation of the mTOR pathway is required for PEMF-stimulated osteogenic differentiation.

Mouse (Murine) Mechanistic Target of Rapamycin (serine/threonine Kinase) (FRAP1) interaction partners

1. this work revealed that SNX10 controls mTOR activation through regulating chaperone-mediated autophagy-dependent amino-acid metabolism.

2. SAM68 interaction with U1A modulates U1 snRNP recruitment and regulates mTor pre-mRNA splicing.

3. Targeting mTOR and Src restricts hepatocellular carcinoma growth in a novel murine liver cancer model.

4. ATF3 deficiency activated mTOR/p70S6K/HIF-1alpha signaling.

5. The hippocampal BDNF-TrkB-mTOR pathway is vital for cannabidiol-induced antidepressant-like effect.

6. These results indicate that miR-181a is involved in hippocampal contextual fear memory by activating the mTOR signaling pathway

7. Study using lung tissue and derived cultured cells from patients with chronic obstructive pulmonary disease (COPD) and from age- and sex-matched control smokers revealed that cell senescence in COPD was linked to mTOR activation, and mTOR inhibition by low-dose rapamycin prevented cell senescence and inhibited the proinflammatory senescence-associated secretory phenotype.

8. Endothelial leptin/Akt/mTor signaling contributes to cardiac fibrosis and functional deterioration by suppressing endothelial autophagy and promoting endothelial dysfunction in a chronic pressure overload model.

9. Palladin operates downstream of mTOR to modulate axon morphogenesis

10. experiments using in vitro ADR-administered Rac1 knockdown podocytes also supported that a reduction in Rac1 suppressed mTOR activity in injured podocytes. Taken together, these data indicate that Rac1-associated mTOR activation in podocytes plays an important role in preventing the kidneys from developing glomerulosclerosis.

11. results demonstrate that suppression of the IGF-1R/mTOR-pathway by EGFR/ERK/IGFBP-3 signaling is necessary for balanced osteoblast maturation providing a mechanism for the skeletal phenotype observed in EGFR-deficient mice.

12. Stage-dependent therapeutic efficacy in PI3K/mTOR-driven squamous cell carcinoma of the skin.

13. these studies demonstrate altered Kv1.1 protein expression in association with mTOR hyperactivation in NS-Pten KO mice and suggest a role for mTOR signaling in the modulation of voltage-gated ion channel expression in this model.

14. BCAP is critical for IL-1R-induced phosphoinositide 3-kinase-Akt-mechanistic target of rapamycin (mTOR) activation, and minimal inhibition of mTOR completely abrogated IL-1beta-induced differentiation of pathogenic Th17 cells, mimicking BCAP deficiency.

15. Adipocyte-specific DKO of Lkb1 and mTOR protects mice against HFD-induced obesity, but results in insulin resistance

16. mTOR plays a crucial role in regulation of M2 macrophage polarization and direct the innate immune homeostasis during Leishmania infection.

17. Disruption of neuronal ciliogenesis by somatic MTOR mutations underlies cortical dyslamination in focal malformations of cortical development (FMCDs). Accumulation of OFD1 at centriolar satellites due to perturbed autophagy was responsible for the defective neuronal ciliogenesis. Disrupted neuronal ciliogenesis accounted for cortical dyslamination in FMCDs by compromising Wnt signals essential for neuronal polarization.

18. Loss of mTORC1 signaling by removal of Raptor in tendons caused severe tendon defects postnatally.

19. These results suggest that PTEN persistently suppresses OL development in an mTOR-independent manner, and at least in part, via controlling GSK3beta activity. OPC-targeted PTEN-GSK3beta inactivation may benefit facilitated OL regeneration and myelin repair.

20. UCH-L1 bypasses mTOR to promote protein biosynthesis and is required for MYC-driven lymphomagenesis in mice.

Zebrafish Mechanistic Target of Rapamycin (serine/threonine Kinase) (FRAP1) interaction partners

1. This study reveals the dramatic rescue effects of L-leucine stimulation of mTORC1 in RBS cells and supports that normal gene expression and translation requires ESCO2 function.

2. By inhibiting mTOR signaling via Fbxw7, the amount of myelination during development is reduced.

3. up-regulated in model of hepatic steatosis

4. Apc mutations activate mechanistic target of rapamycin complex 1 in mice and zebrafish

5. In our zebrafish model, autophagy induction does not depend on inhibition of the Tor pathway or activation of Tp53.

6. TOR signaling is a common pathological pathway that can be leveraged for therapeutic benefits in cardiomyopathies of different origins.

7. in addition to regulating cell growth and proliferation, TOR signaling controls the developmental program guiding epithelial morphogenesis in the intestine

Pig (Porcine) Mechanistic Target of Rapamycin (serine/threonine Kinase) (FRAP1) interaction partners

1. The addition of methionine source mixes in porcine mammary tissue slices improves the abundance of phosphorylated-mechanistic target of rapamycin (P-mTOR) and mTOR. However, the abundance of P-mTOR and mTOR proteins is not affected by the addition of single methionine sources. mTORC1 protein synthesis in porcine mammary glands is regulated by the local available methionine depending on methionine sources.

2. The immunoprecipitation results also showed that high AA concentrations significantly increased the interaction of mTOR and PPARg. In summary, PPARg plays an important role in the regulation of IGF-1 secretion and gene expression in response to dietary protein.

3. 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-mTOR-FOXO1 signaling and suppressing the activation of TLR4 and/or NOD2 signaling pathways.

4. In summary, mTORC1 signaling is a key mechanism of PARylation-autophagy and its inhibition improved developmental ability and embryo quality by promoting selective autophagic degradation of ubiquitinated aggregates in porcine blastocysts.

5. Data show that the amount of proteins related to mechanistic target of rapamycin (mTOR) signaling pathways decreased along crypt-villus axis (CVA).

6. AMPK-mTOR-autophagy signaling is altered by intrauterine growth restriction in newborn piglets.

7. Uroguanylin modulates (Na++K+)ATPase in a proximal tubule cells via cGMP/protein kinase G, cAMP/protein kinase A, and mTOR pathways.

8. mTOR is involved in 17beta-estradiol-induced, cultured immature boar Sertoli cell proliferation via regulating the expression of SKP2, CCND1, and CCNE1.

9. L-Glutamine enhances enterocyte growth via activation of the mTOR.

10. Arg, Leu, and Gln act coordinately to stimulate proliferation of pTr cells through activation of the MTOR-RPS6K-RPS6-EIF4EBP1 signal transduction pathway.

11. Data indicate that the expression of MAP1LC3A, B and autophagy-associated genes (ATG5, mTOR, Beclin-1) was increased in normal pigs, while decreased in miniature pigs.

12. Biochemical, cellular, and molecular data suggest that L-arginine stimulates mTOR biosynthesis, mTOR signaling, and overall protein biosynthesis/turnover in placental/trophoblast and blastocyst/ectoderm cells thereby enhancing cell proliferation.

13. Porcine circovirus type 2 (PCV2) might induce autophagy via the AMPK/ERK/TSC2/mTOR signaling pathway in the host cells, representing a pivotal mechanism for PCV2 pathogenesis

14. Enteral leucine supplementation increases protein synthesis in skeletal and cardiac muscles and visceral tissues of neonatal pigs through mTORC1-dependent pathways

15. These results suggest that feeding stimulates mTORC1 signaling in muscle and viscera, but mTORC1 activation alone is not sufficient to stimulate PS in all tissues.

16. Findings illustrate a mechanism for the cardioprotective effects of lovastatin through inhibition of Rheb and mTORC1 and promotion of a differentiated vascular smooth muscle cell phenotype.

Cow (Bovine) Mechanistic Target of Rapamycin (serine/threonine Kinase) (FRAP1) interaction partners

1. Overall, data indicate that mTOR and insulin signaling pathways in adipose tissue adapt to the change in physiologic state during the periparturient period.

2. U2AF65 functions as a positive regulator of milk synthesis in and proliferation of bovine mammary epithelial cells via the mTOR-SREBP-1c signalling pathway.

3. The role of the PI3K/Akt/mTOR pathway in inflammatory regulation is independent of the activation of TLRs/NF-kappaB. Cross-talk between PI3K/Akt/mTOR and TLRs/NF-kappaB signaling pathways promote inflammation.

4. AnxA2 functions as a critical regulator for amino acid or hormone-induced milk synthesis and mammary gland epithelial cell proliferation via the PI3K-mTOR-SREBP-1c/Cyclin D1 signaling pathway.

5. 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.

6. 14-3-3gamma affects mTOR protein pathway and regulates lactogenesis in dairy cow mammary epithelial cells.

7. Methionine promoted casein synthesis, and this may be mediated by enhanced intracellular substrate availability and by activating JAK2-STAT5 and mTOR signaling pathways.

8. Insulin-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.

9. IGF-I down-regulated functional IGF-I receptor via GSK-3beta inhibition and mTOR activation; constitutive activity of GSK-3beta maintained IGF-I receptor level in nonstimulated cells.

10. stimulation of mammary protein synthesis by amino acids and its enhancement by a combination of the lactogenic hormones hydrocortisone, insulin, and prolactin were associated with increased phosphorylation of the mTOR substrates

11. data demonstrate that hypoxia-induced adventitial fibroblast proliferation requires activation and interaction of PI3K, Akt, mTOR, p70S6K, and ERK1/2.

12. prostaglandin F2alpha phosphorylates TSC2 and activates mTOR and ribosomal protein S6 kinase signaling in an AKT-independent manner

13. mTOR links IGF-I and EGF signaling in inhibiting the autophagy pathways.