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. Collectively, these data uncover a functional key role of the PI3K/mTORC2/AKT signaling cascade for viral oncogene repression in hypoxic human papilloma virus-positive cancer cells and provide new insights into the poorly understood cross talk between oncogenic human papilloma viruses and their host cells under hypoxia.

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. Studies indicate that mTOR serine-threonine kinase (mTOR) plays a role in regulating survival, proliferation and migration processes in cancer [Review].

4. The findings revealed that delayed endothelial replicative senescence caused by the inhibition of MTORC1 activation could be modulated by miR-107 via its influence on PTEN.

5. Proliferation of PC cells by targeting the c-Met/Akt/mTOR signaling pathway.

6. Analysis of tumor samples with reduced expression of the VEGFA gene revealed association of increased expression of RAF1 and mTOR genes with metastasis.

7. Study shows high phosphorylated-mammalian target of rapamycin expression is associated with recurrence and shorter disease-free survival in atypical meningiomas.

8. describe a leucine- and Rag-independent mechanism of mTORC1 activation by glutamine that depends on phospholipase D and the production of phosphatidic acid, which is required for the stability and activity of mTORC1

9. p-mTOR overexpression was independently associated with poor prognosis in patients with tongue SCC. Inhibition of mTOR activity showed the promising activity in tongue SCC cell lines and mouse model.

10. MYO18B promoted hepatocellular carcinoma growth and migration via the activation of PI3K/AKT/mTOR signaling pathway.

11. Targeting mTOR with rapamycin may significantly potentiate the inhibitory effect in BAG1silenced cells.

12. The importance of the SPAG5/AKT-mTOR/Wnt3 axis identified in BUC cell models.

13. These results pinpoint mTOR as a mechanism of resistance to chemotherapy in KRAS-mutant lung cancer and validate a rational and readily translatable strategy that combines mTOR inhibitors with standard chemotherapy to treat KRAS-mutant adenocarcinoma, the most common and deadliest lung cancer subset.

14. the results indicated that JB inhibits glycolysis by down-regulating HK2 expression through inactivating the Akt/mTOR pathway in non-small cell lung cancer (NSCLC) cells, suggesting that JB might be a potential therapeutic agent for the treatment of NSCLC.

15. On title.

16. Silencing lncDDIT4 in naive CD4(+) T cells enhanced Th17 differentiation through increased activation of the DDIT4/mTOR pathway.

17. we evaluated the link between mTOR kinase activity and the level of LDH expression / function. Furthermore, we elaborated the metabolic changes produced in cells by the mTOR-directed LDH-A up-regulation. Interestingly, we observed that in the non-neoplastic MCF-10A culture, mTOR-directed up-regulation of LDH-A was followed by a reprogramming of cell metabolism, which showed an increased dependence on glycolysis rather tha

18. Data reveal that LAT2 functions as an oncogenic protein and could regulate glutamine-dependent mTOR activation to promote glycolysis and decrease GEM sensitivity in pancreatic cancer.

19. patients with a high p-mTOR (HR 1.27, p = 0.21). CONCLUSIONS: Phosphorylated mTOR is differentially expressed in localized RCC and metastasis. Elevated phosphorylation of mTOR is associated with aggressive pathologic features and unfavorable outcome

20. This review is an emerging evidence that mTOR-dependent brain vascular dysfunction, a universal feature of aging, may be one of the mechanisms linking the regulation of the rate of aging to the pathogenesis of Alzheimer's disease. [review]

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

1. findings strongly suggest that mTOR inhibition during T. cruzi infection induces NLRP3 inflammasome activation and mtROS production, resulting in an inflammatory-like macrophage profile that controls T. cruzi replication.

2. MTOR is essential for thymic epithelial cells development and maturation by regulating proliferation and WNT signaling activity through autophagy

3. targeting mTORC2 retards fibroblast activation and kidney fibrosis through suppressing Yap/Taz activation.

4. study demonstrated that AKT-mTOR axis is a key mediator of tendon differentiation and provided a novel therapeutic target for tendinopathy and tendon injuries.

5. Here the authors report that Ube3a regulates mTORC1 signaling by targeting p18, a subunit of the Ragulator. Ube3a ubiquitinates p18, resulting in its proteasomal degradation.

6. The data identify a novel connection, although not elucidated at the molecular level, between mTORC1 and cathepsin activity in a manner relevant to MZ dynamics.

7. These results pinpoint mTOR as a mechanism of resistance to chemotherapy in KRAS-mutant lung cancer and validate a rational and readily translatable strategy that combines mTOR inhibitors with standard chemotherapy to treat KRAS-mutant adenocarcinoma, the most common and deadliest lung cancer subset.

8. To regulate both TLR4-MyD88 and mTOR-autophagy pathways.

9. Study provides novel insight into how altered mTOR signaling is linked to Alzheimer's disease (AD) pathology, without the use of an in-vivo AD model that already displays neuropathological hallmarks of the disease.

10. Tsc1 ablation in Schwann cell progenitors in mice resulted in activation of mTOR signaling, and caused over-proliferation of Schwann cells and blocked their differentiation, leading to hypomyelination. Transcriptome profiling analysis revealed that mTOR activation in Tsc1 mutants resulted in upregulation of a polo-like kinase (PLK)-dependent pathway and cell cycle regulators.

11. Blocking TLR4/Akt/mTOR might be an underlying basis for the anti-inflammatory effect of 20C.

12. These results strongly suggest that HSP22 interacts with mTOR and regulates TNF-alpha-induced IL-6 synthesis in osteoblasts.

13. results suggest that loss of mTOR in the Ventral Tegmental Area shifts the balance of excitatory and inhibitory synaptic transmission and decreases dopamine release and reuptake in the Nucleus Accumbens.

14. This study identified GSK3beta as a positive regulator of prosurvival signaling, including the mTOR pathway.

15. These results provide evidence of involvement of the mTORC1-HIF-1alpha pathway in burn-induced metabolic derangements.

16. Treatment with ATP induced the increase in [Ca(2+)]i through the P2Y receptor/inositol 1,4,5-trisphosphate receptor pathway, and subsequent activation of mTOR in vitro.

17. Gal8 inhibits mTOR activity through its Ragulator-Rag signaling machinery.

18. Study data demonstrate that mTOR functions mediated by mTORC1 are indispensable for multiple processes of neural crest cells (NCCs) development including proliferation, survival, and differentiation during craniofacial morphogenesis and organogenesis, and P53 hyperactivity in part accounts for the defective craniofacial development in NCC-mTOR knockout mice.

19. Study identified a novel specific molecular link between maternal folate availability and fetal growth, involving regulation of placental mTOR signaling by folate, resulting in changes in placental nutrient transport.

20. mTOR is a critical mediator of blood-brain barrier breakdown in models of Alzheimer's disease and vascular cognitive impairment.

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

2. 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.

3. 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.

4. 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.

5. 14-3-3gamma affects mTOR protein pathway and regulates lactogenesis in dairy cow mammary epithelial cells.

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

7. 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.

8. 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.

9. 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

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

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

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