mTOR Antibody - #AF6308

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产品: mTOR 抗体
货号: AF6308
描述: Rabbit polyclonal antibody to mTOR
应用: WB IHC IF/ICC
文献验证: WB, IHC
反应: Human, Mouse, Rat, Fish
预测: Pig, Bovine, Horse, Sheep, Rabbit, Dog, Chicken
蛋白号: P42345
RRID: AB_2835169

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   规格 价格 库存
 50ul RMB¥ 1250 现货
 100ul RMB¥ 2300 现货
 200ul RMB¥ 3000 现货

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说明书
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实验方案
WB Handbook
IHC Protocol
IF/ICC Protocol

产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human, Mouse, Rat, Fish
克隆:
Polyclonal
特异性:
mTOR Antibody detects endogenous levels of total mTOR.
RRID:
AB_2835169
引用格式: Affinity Biosciences Cat# AF6308, RRID:AB_2835169.
偶联:
Unconjugated.
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

dJ576K7.1 (FK506 binding protein 12 rapamycin associated protein 1); 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; FK506-binding protein 12-rapamycin complex-associated protein 1; FKBP rapamycin associated protein; FKBP12 rapamycin complex associated protein; FKBP12-rapamycin complex-associated protein 1; FKBP12-rapamycin complex-associated protein; FLJ44809; FRAP; FRAP1; FRAP2; Mammalian target of rapamycin; Mechanistic target of rapamycin; mTOR; MTOR_HUMAN; OTTHUMP00000001983; RAFT1; Rapamycin and FKBP12 target 1; Rapamycin associated protein FRAP2; Rapamycin target protein 1; Rapamycin target protein; RAPT1; Serine/threonine-protein kinase mTOR;

抗原和靶标

免疫原:

A synthesized peptide derived from human mTOR, corresponding to a region within C-terminal amino acids.

基因/基因ID:
MTOR(2475)
描述:
an atypical kinase belonging to the PIKK family of kinases. Controls cell growth through protein synthesis regulation. Downstream of PI3K/Akt pathway and required for cell survival. Acts as the target for the cell-cycle arrest and immunosuppressive effects of the FKBP12-rapamycin complex.

研究领域

· Cellular Processes > Transport and catabolism > Autophagy - other.   (View pathway)

· Cellular Processes > Transport and catabolism > Autophagy - animal.   (View pathway)

· Cellular Processes > Cell growth and death > Cellular senescence.   (View pathway)

· Environmental Information Processing > Signal transduction > ErbB signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > HIF-1 signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Phospholipase D signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > mTOR signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > AMPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Apelin signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Jak-STAT signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > EGFR tyrosine kinase inhibitor resistance.

· Human Diseases > Drug resistance: Antineoplastic > Endocrine resistance.

· Human Diseases > Endocrine and metabolic diseases > Type II diabetes mellitus.

· Human Diseases > Endocrine and metabolic diseases > Insulin resistance.

· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Proteoglycans in cancer.

· Human Diseases > Cancers: Overview > MicroRNAs in cancer.

· Human Diseases > Cancers: Specific types > Colorectal cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Pancreatic cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Glioma.   (View pathway)

· Human Diseases > Cancers: Specific types > Prostate cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Acute myeloid leukemia.   (View pathway)

· Human Diseases > Cancers: Specific types > Breast cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Hepatocellular carcinoma.   (View pathway)

· Human Diseases > Cancers: Specific types > Gastric cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Central carbon metabolism in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Choline metabolism in cancer.   (View pathway)

· Organismal Systems > Aging > Longevity regulating pathway.   (View pathway)

· Organismal Systems > Aging > Longevity regulating pathway - multiple species.   (View pathway)

· Organismal Systems > Immune system > Th17 cell differentiation.   (View pathway)

· Organismal Systems > Endocrine system > Insulin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Thyroid hormone signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Adipocytokine signaling pathway.

文献引用

1). Aberrant translation regulated by METTL1/WDR4‐mediated tRNA N7‐methylguanosine modification drives head and neck squamous cell carcinoma progression. Cancer Communications, 2022 (PubMed: 35179319) [IF=16.2]

Application: WB    Species: Mice    Sample: METTL1‐KO cells

FIGURE 4 METTL1‐mediated m7G tRNA modification regulates the activity of the PI3K/AKT/mTOR signaling pathway. (A) Scatterplot of the TRs in METTL1‐WT and METTL1‐KO SCC15 cells. TRs were calculated by dividing the ribosome‐binding transcript signals by input RNA‐seq signals. (B) KEGG pathway analysis of the genes with decreased TRs upon METTL1 knockout. (C) The PI3K/AKT/mTOR signaling pathway was enriched in RNC‐seq datasets by GSEA (NES = 1.64, FDR = 0.165, P < 0.001). (D) Western blotting of PI3K/AKT/mTOR signaling pathway proteins and downstream proteins using the indicated antibodies. (E) qRT‐PCR analysis of PIK3CA with RNC and input samples in SCC9 and SCC15 cells. (F) The protein levels of PI3K, AKT, and p‐AKT in METTL1‐WT, METTL1‐KO, PI3K‐transfected METTL1‐KO cells (KO + PIK3CA) and 5 μg/mL SC79‐treated METTL1‐KO cells cultured with (KO + SC79). (G‐I) The proliferation (G), migration (H) and invasion abilities (I) were partially restored after transfecting METTL1‐KO cells with the PI3K plasmid or activating AKT. Data are presented as the mean ± SD and analyzed by Student's t‐test. *, P < 0.05, **, P < 0.01, ***, P < 0.001. Abbreviations: PI3K/AKT/mTOR: phosphatidylinositol‐3‐kinase/protein kinase B/mammalian target of rapamycin; METTL1: Methyltransferase‐like 1; WT: wild‐type; KO: knockout; TRs: translation ratios; KEGG: Koto Encyclopedia of Genes and Genomes; GSEA: gene set enrichment analysis; NES: normalized enrichment score; FDR: false discovery rate; qRT‐PCR: quantitative real‐time PCR; RNC: Ribosome nascent‐chain complex‐bound; MMP9: matrix metalloprotein 9; Bcl‐2: B‐cell lymphoma‐2; P‐S6K: phosphorylation of S6 kinase; BAX: Bcl‐2‐associated X protein; PIK3CA: phosphatidylinositol‐4,5‐bisphosphate 3‐kinase, catalytic subunit alpha; SD: standard deviation
2). Rationally designed rapamycin-encapsulated ZIF-8 nanosystem for overcoming chemotherapy resistance. BIOMATERIALS, 2020 (PubMed: 32841911) [IF=12.8]

Application: WB    Species: human    Sample: MCF-7/ADR cells

Figure 2.(b) ZIF-8 (10 µg mL−1, 24 h) did not inhibit p70S6K phosphorylation at Thr389 and mTOR phosphorylation at Ser2448 but induced the accumulation of LC3-II, suggesting ZIF-8 elicited mTOR-independent autophagy.
3). Polystyrene nanoplastics promote colitis-associated cancer by disrupting lipid metabolism and inducing DNA damage. Environment international, 2025 (PubMed: 39805171) [IF=10.3]
4). MiR-146b-5p enriched bioinspired exosomes derived from fucoidan-directed induction mesenchymal stem cells protect chondrocytes in osteoarthritis by targeting TRAF6. Journal of nanobiotechnology, 2023 (PubMed: 38105181) [IF=10.2]

Application: WB    Species: Rat    Sample: chondrocytes

Fig. 7 Enriched miR-146b-5p in F-MSCs-Exo inhibits PI3K/AKT/mTOR pathway by targeting TRAF6. (A, B) Western blot analysis was performed to detect the impact of F-MSCs-Exo on TRAF6 and the PI3K/AKT/mTOR pathway in rat chondrocytes. (C, D) The expression of TRAF6 was quantitatively analyzed using immunofluorescence staining and ImageJ software (scale bar = 10 μm). (E, F) Direct visualization of chondrocytes treated with nc-inhibitor and miR-146b-5p-inhibitor was performed using Alcian blue staining and safranin staining. (G, H) Western blot analysis was conducted to examine the expressions of TRAF6 and the PI3K/AKT/mTOR pathway in chondrocytes after treatment with nc-inhibitor and miR-146b-5p-inhibitor. (ns, no significant difference; *p 
5). Morphine-induced microglial immunosuppression via activation of insufficient mitophagy regulated by NLRX1. Journal of Neuroinflammation, 2022 (PubMed: 35414088) [IF=9.3]
6). NCAPD2 inhibits autophagy by regulating Ca2+/CAMKK2/AMPK/mTORC1 pathway and PARP-1/SIRT1 axis to promote colorectal cancer. CANCER LETTERS, 2021 (PubMed: 34229059) [IF=9.1]

Application: WB    Species: Human    Sample: CRC cells

Fig. 2. NCAPD2 inhibited cell autophagy and disrupted autophagic flux via Ca2+/CAMKK2/AMPK/mTORC1 pathway. (A) Western blot analyses for phosphorylated mTOR (p-mTOR, S2448), phosphorylated p70S6K (p-p70S6K, T389/412), phosphorylated 4E-BP1 (p-4E-BP1, T70) and phosphorylated AKT (p-AKT, S473) in CRCC cells with different treatments as indicated. (B) Western blot of indicated proteins in cells treated with mTORC1 inhibitor Rapamycin (3 nM, 24h). (C) Immunofluorescence staining of LC3II (red) and P62 (red) in CRC cells with different treatments as indicated. Merged images represented overlays of LC3II or P62 and nuclear staining by DAPI (blue). (D) Intracellular Ca2+ levels were analyzed by flow cytometry after staining with the fluorescent probe Fluo-3, AM in CRC cells. (E) Representative Western blot gel documents of phosphorylated CAMKK2(S511), phosphorylated AMPK(T172), phosphorylated mTOR(S2448), Beclin, ATG5, P62, LC3II in CRC cells with different treatments. (F) Western blots of indicated proteins in cells treated with an inhibitor of microsomal Ca2+-ATPase Thapsigargin (1 μM, 6h) and Ca2+ chelator BAPTA-AM (10 μM, 12h) respectively. Results are shown as mean ± s.d, *P < 0.05, **P < 0.01, ***P < 0.001, based on Student’s t-test. . (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
7). Suppression of steroid 5α-reductase type I promotes cellular apoptosis and autophagy via PI3K/Akt/mTOR pathway in multiple myeloma. Cell Death & Disease, 2021 (PubMed: 33627630) [IF=8.1]

Application: WB    Species: human    Sample: ARP1 and H929 cells

Fig. 7 |Dutasteride possesses a therapeutic effect on MM.A MTT proliferation assay of ARP1 and H929 cells treated with different concentrations of dutasteride for 48 or 72 h. B Expression of apoptosis markers in dutasteride-treated ARP1 and H929 cells as determined by western blotting analysis. C Western blotting showed that Dutasteride treatment inhibited the activity of PI3K/Akt/mTOR signaling in ARP1 and H929 cells.
8). Polysaccharide from Strongylocentrotus nudus eggs regulates intestinal epithelial autophagy through CD36/PI3K-Akt pathway to ameliorate inflammatory bowel disease. International Journal of Biological Macromolecules, 2023 (PubMed: 37327932) [IF=7.7]
9). Insulin promotes the bone formation capability of human dental pulp stem cells through attenuating the IIS/PI3K/AKT/mTOR pathway axis. Stem cell research & therapy, 2024 (PubMed: 39075596) [IF=7.5]

Application: WB    Species: Human    Sample: DPSCs

Fig. 5 LY294002 attenuates the responsiveness of 10− 6 M insulin to the IIS/PI3K/AKT/mTOR pathway axis in human DPSCs. A LY294002 attenuated the inhibiting effect of 10− 6 M insulin on the protein expressions of INSR, IGF1R, and IRS1 in DPSCs at day 7. B and C LY294002 attenuated the responsiveness of 10− 6 M insulin to the PI3K/AKT pathway in DPSCs at day 7. D LY294002 attenuated the promoting effect of 10− 6 M insulin on the protein expression of mTOR in DPSCs at day 7. Representative western blotting (left) and quantification analysis (right). Data are expressed as the mean ± SD of n = 3. Full-length blots/gels are presented in Supplementary Figs. 3–6. *P 
10). Anti-b diminishes hyperlipidaemia and hepatic steatosis in hamsters and mice by suppressing the mTOR/PPARγ and mTOR/SREBP1 signalling pathways. British journal of pharmacology, 2024 (PubMed: 39614407) [IF=7.3]
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