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. 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.

2. 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.

3. 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

4. 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]

5. Our data demonstrate that mTOR signaling is significantly dysregulated in human temporal lobe epilepsy

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

7. Findings show that high expression of the angiogenic marker, VEGF, in visceral adipocytes directly promotes vasculature in the uterus and mTOR activity in the endometrial glands, and provide evidence that VEGF-mTOR signaling drives endometrial cell growth leading to hyperplasia and cancer.

8. Data suggest that ORP5/OSBPL5 promotes cell proliferation, cell motility, and invasiveness of neoplasm cells; this effect of ORP5/OSBPL5 depends on functional OSBP-related domain (ORD). ORP5/OSBPL5 is needed for activation of mTORC1 signaling and for transport of mTOR to lysosomes. (OSBPL5 = oxysterol-binding protein-related protein-5)

9. evidence of how HMGB proteins contribute to ribosome-biogenesis control, with special emphasis on a common nexus to the target of rapamycin (TOR) pathway, a signaling cascade essential for cell growth and proliferation from yeast to human.

10. Silencing of TRPC5 and inhibition of autophagy reverses adriamycin drug resistance in breast carcinoma via CaMKKbeta/AMPKalpha/mTOR pathway.

11. L-type amino acid transporter 1 (LAT1) inhibitor, BCH reduces the phosphorylation of mechanistic target of rapamycin kinase (mTOR) in fibroblast-like synoviocytes from patients with rheumatoid arthritis. mTOR inhibitor, temsirolimus, neutralizes the stimulation of interleukin-17 on LAT1.

12. These results indicate that, under stressful conditions, maintained mTORC1 signaling in cancer cells promotes survival by suppressing endogenous DNA damage, and may control cell fate through the regulation of CHK1.

13. Results demonstrated that ASCT2 and pmTOR protein levels were significantly higher in epithelial ovarian cancer (EOC) tissues and predicting a poor prognosis. The expression levels of ASCT2 and pmTOR in EOC were positively correlated indicating a synergistic effect on the growth and development of early EOC.

14. DEPTOR interaction with mTOR represses its kinase activity and rewires the mTOR signaling pathway. [review]

15. both SphK1 overexpression and S1P addition increased mTOR phosphorylation as shown by ELISA, while S1PR2 inhibition had the inverse effect. These data suggest that CerS6 and SphK1 regulate mTOR signaling in breast cancer cell proliferation. Moreover, mTOR activity can be regulated by the balance between S1P and C16ceramide, which is generated by CerS6.

16. Study demonstrate that the miR-495 exerts promotive effects on GC chemosensitivity via inactivation of the mTOR signaling pathway by suppressing ERBB2. The study provides reliable evidence supporting the use of miR-495 as a novel potential target in the chemotherapy of GC.

17. a functional convergence between the mTOR pathway and IFITM3 proteins at endolysosomal membranes.

18. data on TFEB nucleo-cytoplasmic shuttling suggest an unpredicted role of mTOR in nuclear export.

19. In this review, we assess the use of mTOR inhibitors to treat age-related pathologies, discuss possible molecular mechanisms of action where evidence is available, and consider strategies to minimize undesirable side effects.

20. The expression of CXCR4 and mTOR were found to be negatively correlated with remission. Kaplan-Meier analysis indicated a significant decrease in the rate of progression-free survival (PFS) and in that of overall survival (OS) in patients positive for CXCR4 and mTOR expression.

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

1. 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.

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

3. 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.

4. 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.

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

6. The authors demonstrate that in primary osteoclasts, mTOR is localized on the lysosomal surface even when mTOR activity is inhibited. Their findings reveal that mTOR targeting to the lysosome in osteoclasts is activity-independent, and that its disassociation from the lysosome during starvation is not universal.

7. studies suggest that mTOR regulates vascular integrity and function and that mTOR attenuation may restore neurovascular function and cardiovascular health

8. Decreased liver mRNA levels for multiple genes associated with mTOR signaling and oxidative stress parameters were detected in aldh5a1(-/-) mice, and several were significantly improved with the administration of mTOR inhibitors (Torin 1/Torin 2).

9. Results suggest that activation of mammalian target of rapamycin (mTOR)/reactive oxygen species (ROS)/NOD-like receptor protein 3 (NLRP3) signaling may contribute to the development of systemic lupus erythematosus (SLE).

10. mTOR coordinates transcriptional and metabolic programs in activated Regulatory T cell subsets to mediate tissue homeostasis.

11. Regnase-1 predominantly regulates mTORC1 signaling.

12. Study shows that GLP-1 receptor signalling promotes beta-cell glucose metabolism via mTOR-dependent HIF-1alpha activation. findings suggest that chronic GLP-1 actions on insulin secretion include elevated beta-cell glucose metabolism. Moreover, our data reveal novel aspects of GLP-1 stimulated insulin secretion involving de novo gene expression.

13. metabolic profiling reveals elevated glycolysis and increased mTORC1 signaling in Ndfip1-deficient Treg cells

14. Sesn2/AMPK/mTOR signaling mediates balance between survival and apoptosis in sensory hair cells under stress.

15. mTOR is a direct interacting partner of Trx1 in the heart. Trx1 protects cardiomyocytes against oxidative stress by reducing mTOR at Cys-1483, thereby preserving the activity of mTOR and inhibiting cell death.

16. the present study suggested that Pulsed electromagnetic fields (PEMFs) reduced osteoclast formation from RAW264.7 macrophages via inhibition of the Akt/mTOR signaling pathway. These findings provided novel insight into the mechanisms through which PEMFs suppress osteoclast differentiation.

17. mTOR signaling is a key mediator of central insulin dysfunction, which leads to pathogenesis of Alzheimer disease.

18. Results indicate that L-Arg stimulates protein synthesis via the activation of the mTOR (Thr 2446)/p70S6K signaling pathway in an NO-dependent manner.

19. High mTOR expression is associated with cardiac hypertrophy.

20. cPKC&-gamma modulated sequential reactivation of mTOR inhibited autophagic flux in neurons exposed to OGD/R, which may provide endogenous interventional strategies for stroke, especially ischemia/reperfusion injury

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. 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.

2. 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.

3. 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.

4. 14-3-3gamma affects mTOR protein pathway and regulates lactogenesis in dairy cow mammary epithelial cells.

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

6. 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.

7. 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.

8. 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

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

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

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