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primary antibodies against mtor  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc primary antibodies against mtor
    Primary Antibodies Against Mtor, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 3879 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+antibodies+against+mtor/mTOR+Rabbit+mAb/pm41277553-202-0-51
    Average 97 stars, based on 3879 article reviews
    primary antibodies against mtor - by Bioz Stars, 2026-11
    97/100 stars

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    Related Articles

    Western Blot:

    Article Title: Endurance exercise with reduced muscle glycogen content influences substrate utilization and attenuates acute mTORC1- and autophagic signaling in human type I and type II muscle fibers
    Article Snippet: .. For immunoblotting, primary antibodies against mTOR (Ser 2448 , #2971; total, #2983), 4E-BP1 (Thr 37/46 , #2855; total, #9644), eEF2 (Thr 56 , #2331; total, #2332), S6K1 (Thr 389 , #9234; total #2708, ACC (Ser 79 , #3661; total, #3676), AMPK (Thr 172 , #4188; total, #2532), ULK1 (Ser 555 , #5869; total, #8054), LC3B (#2775), and COX IV (#4860) were purchased from Cell Signaling Technology (Beverly, MA, USA). .. Primary antibody for total MuRF-1 (#sc-398608) and UBR5 (#sc-515494) were purchased from Santa Cruz Biotechnology (Heidelberg, Germany).

    Article Title: Endurance exercise with reduced muscle glycogen content influences substrate utilization and attenuates acute mTORC1- and autophagic signaling in human type I and type II muscle fibers
    Article Snippet: .. For immunoblotting, primary antibodies against mTOR (Ser 2448 , #2971; total, #2983), 4E-BP1 (Thr 37/46 , #2855; total, #9644), eEF2 (Thr 56 , #2331; total, #2332), S6K1 (Thr 389 , #9234; total #2708), ACC (Ser 79 , #3661; total, #3676), AMPK (Thr 172 , #4188; total, #2532), ULK1 (Ser 555 , #5869; total, #8054), LC3B (#2775), and COX IV (#4860) were purchased from Cell Signaling Technology (Beverly, MA, USA). .. Primary antibody for total MuRF-1 (#sc-398608) and UBR5 (#sc-515494) were purchased from Santa Cruz Biotechnology (Heidelberg, Germany).

    Article Title: Endurance exercise with reduced muscle glycogen content influences substrate utilization and attenuates acute mTORC1- and autophagic signaling in human type I and type II muscle fibers.
    Article Snippet: .. For immunoblotting, primary antibodies against mTOR (Ser2448, #2971; total, #2983), 4E-BP1 (Thr37/46, #2855; total, #9644), eEF2 (Thr56, #2331; total, #2332), S6K1 (Thr389, #9234; total #2708), ACC (Ser79, #3661; total, #3676), AMPK (Thr172, #4188; total, #2532), ULK1 (Ser555, #5869; total, #8054), LC3B (#2775), and COX IV (#4860) were purchased from Cell Signaling Technology (Beverly, MA, USA). .. Primary antibody for total MuRF-1 (#sc-398608) and UBR5 (#sc-515494) were purchased from Santa Cruz Biotechnology (Heidelberg, Germany).

    other:

    Article Title: Autophagy-Regulating, Photothermal Polydopamine-Coated, and Photodynamic Zirconium/Porphyrin-Framed Metal–Organic Frameworks for Enhanced Doxorubicin Therapy in Colon Cancer
    Article Snippet: Subsequently, the PVDF membranes were blocked with tris-buffered saline with Tween 20 (TBST) containing 5% skim milk for 1 h and incubated with various primary antibodies against the following: Beclin-1 (Cell Signaling Technology, 3738), Atg7 (Cell Signaling Technology, 2631), LC3B (Cell Signaling Technology, 3868S), p62 (Cell Signaling Technology, 16177), mamalian target of rapamycin (mTOR, Cell signaling Technology, 2972), phospho-mTOR (Cell Signaling Technology, 2971), and β-actin (Cell Signaling Technology, 4970) overnight at 4 °C.

    Incubation:

    Article Title: Endothelial GTPBP3 directs developmental angiogenesis and neovascularization after limb ischemia via the mtROS/HRl/ATF4/mTORC1 axis.
    Article Snippet: Angiogenesis is a complex energy-demanding process involving the migration and proliferation of endothelial cells (ECs) and microvessel morphogenesis under physiological and pathological conditions, such as embryonic development, neovascularization after ischemia, and tumor growth.. ECs possess remarkable functional plasticity, allowing them to switch rapidly from a quiescent to an active migratory and proliferative state during angiogenesis [1].. A more detailed understanding of the mechanisms underlying this angiogenic switch will facilitate the development of drugs for treating angiogenesis-related diseases.



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    Effects of ANE on <t>mTOR/p70S6K</t> signaling and autophagy in C2C12 myoblasts. (A) The protein levels of p-mTOR, p-p70S6K, p62 and LC3 in C2C12 myoblasts treated with the indicated concentrations (20 and 40 μg/mL) of ANE were measured by Western blotting. (B) Effects of the autophagy inhibitor CQ1 on ANE-treated myoblasts. Representative images of immunofluorescence staining of C2C12 myotubes treated with control medium, CQ1 (5 μM), ANE (40 μg/mL), or ANE (40 μg/mL) combined with CQ1 (5 μM) are shown. The myotubes were stained with an anti-myosin heavy chain antibody (green), and the nuclei were counterstained with DAPI (blue). Scale bar = 100 μm. Quantitative analysis of cell viability and the myotube diameter compared with those of the control cells (bottom panel). The data are presented as the means ± SEMs from three independent experiments, with GAPDH used as the internal control. The data are presented as the means ± SEMs of three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared with the untreated control cells. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    Image Search Results


    Effects of ANE on mTOR/p70S6K signaling and autophagy in C2C12 myoblasts. (A) The protein levels of p-mTOR, p-p70S6K, p62 and LC3 in C2C12 myoblasts treated with the indicated concentrations (20 and 40 μg/mL) of ANE were measured by Western blotting. (B) Effects of the autophagy inhibitor CQ1 on ANE-treated myoblasts. Representative images of immunofluorescence staining of C2C12 myotubes treated with control medium, CQ1 (5 μM), ANE (40 μg/mL), or ANE (40 μg/mL) combined with CQ1 (5 μM) are shown. The myotubes were stained with an anti-myosin heavy chain antibody (green), and the nuclei were counterstained with DAPI (blue). Scale bar = 100 μm. Quantitative analysis of cell viability and the myotube diameter compared with those of the control cells (bottom panel). The data are presented as the means ± SEMs from three independent experiments, with GAPDH used as the internal control. The data are presented as the means ± SEMs of three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared with the untreated control cells. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Journal: Current Research in Toxicology

    Article Title: Areca nut extract exposure disrupts myogenesis and metabolism in C2C12 cells

    doi: 10.1016/j.crtox.2025.100264

    Figure Lengend Snippet: Effects of ANE on mTOR/p70S6K signaling and autophagy in C2C12 myoblasts. (A) The protein levels of p-mTOR, p-p70S6K, p62 and LC3 in C2C12 myoblasts treated with the indicated concentrations (20 and 40 μg/mL) of ANE were measured by Western blotting. (B) Effects of the autophagy inhibitor CQ1 on ANE-treated myoblasts. Representative images of immunofluorescence staining of C2C12 myotubes treated with control medium, CQ1 (5 μM), ANE (40 μg/mL), or ANE (40 μg/mL) combined with CQ1 (5 μM) are shown. The myotubes were stained with an anti-myosin heavy chain antibody (green), and the nuclei were counterstained with DAPI (blue). Scale bar = 100 μm. Quantitative analysis of cell viability and the myotube diameter compared with those of the control cells (bottom panel). The data are presented as the means ± SEMs from three independent experiments, with GAPDH used as the internal control. The data are presented as the means ± SEMs of three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared with the untreated control cells. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Article Snippet: Primary antibodies against p-mTOR (Ser2448), p-p70S6 kinase (Thr389), p62 and LC3-II/LC3-I were purchased from Cell Signaling Technology (Danvers, MA, USA), and the anti-GAPDH antibody was purchased from GeneTex (San Antonio, TX, USA).

    Techniques: Western Blot, Immunofluorescence, Staining, Control

    Schematic illustration of the effects of ANE on C2C12 myoblasts and differentiated myotubes. (A) ANE impairs myogenesis by reducing the differentiation and fusion capabilities of myoblasts, inhibiting p-mTOR/p-P70S6K signaling, and inducing autophagy. In differentiated myotubes, ANE reduces the myotube diameter and MYH4 expression. (B) The metabolomic analysis indicated that ANE may induce metabolic reprogramming in differentiated myotubes, impairing energy production, nitrogen metabolism, and biosynthetic pathways.

    Journal: Current Research in Toxicology

    Article Title: Areca nut extract exposure disrupts myogenesis and metabolism in C2C12 cells

    doi: 10.1016/j.crtox.2025.100264

    Figure Lengend Snippet: Schematic illustration of the effects of ANE on C2C12 myoblasts and differentiated myotubes. (A) ANE impairs myogenesis by reducing the differentiation and fusion capabilities of myoblasts, inhibiting p-mTOR/p-P70S6K signaling, and inducing autophagy. In differentiated myotubes, ANE reduces the myotube diameter and MYH4 expression. (B) The metabolomic analysis indicated that ANE may induce metabolic reprogramming in differentiated myotubes, impairing energy production, nitrogen metabolism, and biosynthetic pathways.

    Article Snippet: Primary antibodies against p-mTOR (Ser2448), p-p70S6 kinase (Thr389), p62 and LC3-II/LC3-I were purchased from Cell Signaling Technology (Danvers, MA, USA), and the anti-GAPDH antibody was purchased from GeneTex (San Antonio, TX, USA).

    Techniques: Expressing