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. Due to regulation of AMPK-/mTOR-mediated autophagy.

3. 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.

4. The overexpression of total and phosphorylated mTOR as well as phosphorylated rpS6 (residues 240-244) were associated with wild-type IDH1 only glioblastomas. The expression and phosphorylation of mTOR and phosphorylation of rpS6 at residues 240-244 were associated with a worse prognosis in glioblastomas.

5. High-expressions of mTOR and 4E-BP1 in patients with extranodal Nasal-type NK/T-cell Lymphoma (ENKTCL) are related to the biological progression and recurrence of ENKTCL

6. Conclusion Rapamycin inhibits cell proliferation and induces autophagy in human neuroblastoma cell lines. The mechanism may be related to suppression of the mTOR signaling pathway

7. our findings indicated that miR-140-5p may inhibit cell growth via blocking c-Met/AKT/mTOR signaling pathway. Collectively, these results suggested that miR-140-5p might be a potential biomarker and target in the diagnosis and treatment of retinoblastoma (RB).

8. Evidence of mTOR pathway activation highlights similarities in the pathogenetic mechanisms underlying gangliogliomas and focal cortical dysplasia, and suggests that mTOR inhibitors may be of utility in ganglioglioma patients with persistent seizures after surgery.

9. To evaluate the association between the five SNPs (mTOR rs2295080 and rs2536, AKT1 rs2494750 and rs2494752, pTEN rs701848) and cancer risk.

10. PI3K/AKT/PTEN/mTOR pathway deregulates frequently in oral carcinomas. mTOR molecule plays a significant role by its overactivation in the corresponding cancer cells by amplifying the signal transduction process to the nucleus.

11. ID activates the canonical VEGF pathway and mTOR in breast tissues.

12. The greater postexercise MPS response with whole egg ingestion is related in part to an enhanced recruitment of mTORC1-Rheb complexes to the lysosome.

13. HSF1 stimulated GLS1-dependent mTOR activation to promote colorectal carcinogenesis.

14. Low Frequency Magnetic Fields Induce Autophagy-associated Cell Death in Lung Cancer through miR-486-mediated Inhibition of Akt/mTOR Signaling Pathway.

15. REVIEW: Oncogenic Roles of the PI3K/AKT/mTOR Axis

16. Our results indicated that the overexpressed TFE3 fusions were capable of escaping from the control by the mTOR signaling pathway and were accumulated in the nucleus in UOK109 and UOK120 cells. The nuclear retention of TFE3 fusions promoted the expression of lysosomal genes and other target genes, facilitating cancer cell resistance against an extreme environment.

17. The activity of the AKT-mTOR-GLI1 axis.

18. The effect on mTOR was not seen with HCQ.

19. A sequence motif search for SOX9-responsive elements identified three motifs in the promoter region of mTOR gene. Study data demonstrate that Hedgehog signaling converges on mTOR via SOX9 and highlight the SOX9-mTOR axis as a viable additional target downstream of smoothened that could enhance tumor elimination in patients with basal cell carcinomas.

20. Circular RNA circNRIP1 acts as a microRNA-149-5p sponge to promote gastric cancer progression via the AKT1/mTOR pathway.

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

1. 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.

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

3. 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.

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

5. deregulation of O-GlcNAcylation affects mTOR signaling activation only in cancer cells. Thus, a crosstalk exists between O-GlcNAcylation and mTOR signaling in contexts of metabolism dysregulation associated to obesity or cancer.

6. Abolished activating transcription factor 6 (ATF6) exacerbated gluconeogenic metabolism by mechanistic target of rapamycin protein (MTOR) mediated down regulation of autophage.

7. These results suggest that glucose supplied from blood vessels might be important for IL-1beta production in tumor-associated macrophages via the integrated signals of the NF-kappaB and mTOR pathways in the tumor microenvironment.

8. work identifies that mTOR is an intrinsic master for monocyte/macrophage development at the early stages through regulating STAT5-IRF8-dependent CD115-expressing pathway.

9. These data suggest that ethanol can acutely prevent the normally observed mTOR-dependent increase in protein synthesis and reduction in autophagy in response to nutrient stimulation, but does not appear to acutely alter proteasome activity.

10. Here we found that mTORC1-deficient mice exhibit normal hippocampal mGluR-LTD and associated behaviors

11. Our results indicate a complex role of mTORC1 in the regulation of cerebral protein synthesis that has not been previously recognized

12. The MPLA-induced activation of glycolytic metabolism in mouse mDC was shown to depend on a JNK-mediated activation of mTOR-signaling, while both MAPK- and NFB-signaling contributed to pro-inflammatory cytokine secretion.

13. mTOR regulates a hyperresponsive state in pulmonary neutrophils late after burn injury.

14. The mTOR-S6K pathway links growth signalling to DNA damage response by targeting RNF168 in embryonic fibroblasts.

15. The present study thus demonstrates that MTOR serves as an early adaptive signal that suppresses the particular matter-induced necroptosis, NFKB activation, and inflammatory response in lung macrophages

16. 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.

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

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

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

20. 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.

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.