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p ser 2448 mtorc1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p ser 2448 mtorc1
    Changes in the phosphorylation of <t>mTORC1-mediated</t> proteins and in the expression of synaptic proteins after DEX exposure. Beginning on DIV 10, the neural spheroids were exposed to 100 μM DEX for 5 days. Western blotting and immunofluorescence were performed using each primary antibody (n = 4 biological replicates). (A) Western blotting revealed the levels of phospho-Ser 2448 -mTORC1 (a), phospho- Thr 37/46 -4E-BP1 (b), and phospho-Thr 389 -p70S6K (c). (B) Western blot analysis and representative images of immunoblots of PSD-95 (a) and GluA1 (b) are shown. Synaptic markers: PSD-95 (green) costained with the neuronal marker MAP-2 (red); GluA1 (green) costained with MAP-2 (red). Scale bar: 100 μm. The data are presented as the means ± standard deviations. mTORC1, mechanistic target of rapamycin complex I; DEX, dexamethasone; DIV, days in vitro; 4E-BP1, eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1; PSD-95, postsynaptic density protein-95; GluA1, AMPA receptor subunit glutamate receptor 1; MAP-2, microtubule-associated protein-2; CON, controls. * p < 0.05 or ** p < 0.01 vs. CON.
    P Ser 2448 Mtorc1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 4770 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p+ser+2448+mtorc1/Phospho-mTOR+(Ser2448)+Antibody/pmc12264662-10-0-4
    Average 97 stars, based on 4770 article reviews
    p ser 2448 mtorc1 - by Bioz Stars, 2026-11
    97/100 stars

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    1) Product Images from "Establishment of a Depression Model Using Dexamethasone-treated Three-dimensional Cultured Rat Cortical Cells"

    Article Title: Establishment of a Depression Model Using Dexamethasone-treated Three-dimensional Cultured Rat Cortical Cells

    Journal: Clinical Psychopharmacology and Neuroscience

    doi: 10.9758/cpn.25.1269

    Changes in the phosphorylation of mTORC1-mediated proteins and in the expression of synaptic proteins after DEX exposure. Beginning on DIV 10, the neural spheroids were exposed to 100 μM DEX for 5 days. Western blotting and immunofluorescence were performed using each primary antibody (n = 4 biological replicates). (A) Western blotting revealed the levels of phospho-Ser 2448 -mTORC1 (a), phospho- Thr 37/46 -4E-BP1 (b), and phospho-Thr 389 -p70S6K (c). (B) Western blot analysis and representative images of immunoblots of PSD-95 (a) and GluA1 (b) are shown. Synaptic markers: PSD-95 (green) costained with the neuronal marker MAP-2 (red); GluA1 (green) costained with MAP-2 (red). Scale bar: 100 μm. The data are presented as the means ± standard deviations. mTORC1, mechanistic target of rapamycin complex I; DEX, dexamethasone; DIV, days in vitro; 4E-BP1, eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1; PSD-95, postsynaptic density protein-95; GluA1, AMPA receptor subunit glutamate receptor 1; MAP-2, microtubule-associated protein-2; CON, controls. * p < 0.05 or ** p < 0.01 vs. CON.
    Figure Legend Snippet: Changes in the phosphorylation of mTORC1-mediated proteins and in the expression of synaptic proteins after DEX exposure. Beginning on DIV 10, the neural spheroids were exposed to 100 μM DEX for 5 days. Western blotting and immunofluorescence were performed using each primary antibody (n = 4 biological replicates). (A) Western blotting revealed the levels of phospho-Ser 2448 -mTORC1 (a), phospho- Thr 37/46 -4E-BP1 (b), and phospho-Thr 389 -p70S6K (c). (B) Western blot analysis and representative images of immunoblots of PSD-95 (a) and GluA1 (b) are shown. Synaptic markers: PSD-95 (green) costained with the neuronal marker MAP-2 (red); GluA1 (green) costained with MAP-2 (red). Scale bar: 100 μm. The data are presented as the means ± standard deviations. mTORC1, mechanistic target of rapamycin complex I; DEX, dexamethasone; DIV, days in vitro; 4E-BP1, eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1; PSD-95, postsynaptic density protein-95; GluA1, AMPA receptor subunit glutamate receptor 1; MAP-2, microtubule-associated protein-2; CON, controls. * p < 0.05 or ** p < 0.01 vs. CON.

    Techniques Used: Phospho-proteomics, Expressing, Western Blot, Immunofluorescence, Marker, In Vitro, Binding Assay

    Schematic diagram showing the molecular mechanisms underlying DEX-induced impaired neuroplasticity. Exposure to DEX downregulates signaling pathways that affect neuroplasticity, including BDNF, sirtuin 1, and mTORC1 signaling. Activation of the mTORC1 signaling pathway induces the synthesis of synaptic proteins as well as BDNF. Secreted BDNF interacts with its receptor TrkB, further activating mTORC1 signaling via PI3K/Akt and MEK/ERK1/2. Therefore, synaptic plasticity is enhanced. Sirtuin 1 is also involved in the regulation of neuroplasticity. The original illustration was created using BioRender (biorender.com). Akt, protein kinase B; AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid; BDNF, brain-derived neurotrophic factor; DEX, dexamethasone; ERK1/2, extracellular signal-regulated kinase 1/2; GluA1, AMPA receptor subunit glutamate receptor 1; MEK, mitogen‑activated protein kinase; mTORC1, mechanistic target of rapamycin complex I; p70S6K, p70S6 kinase; PI3K, phosphatidyl inositol-3 kinase; PSD-95, postsynaptic density protein-95; TrKB, tropomyosin receptor kinase B; 4E-BP1, eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1.
    Figure Legend Snippet: Schematic diagram showing the molecular mechanisms underlying DEX-induced impaired neuroplasticity. Exposure to DEX downregulates signaling pathways that affect neuroplasticity, including BDNF, sirtuin 1, and mTORC1 signaling. Activation of the mTORC1 signaling pathway induces the synthesis of synaptic proteins as well as BDNF. Secreted BDNF interacts with its receptor TrkB, further activating mTORC1 signaling via PI3K/Akt and MEK/ERK1/2. Therefore, synaptic plasticity is enhanced. Sirtuin 1 is also involved in the regulation of neuroplasticity. The original illustration was created using BioRender (biorender.com). Akt, protein kinase B; AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid; BDNF, brain-derived neurotrophic factor; DEX, dexamethasone; ERK1/2, extracellular signal-regulated kinase 1/2; GluA1, AMPA receptor subunit glutamate receptor 1; MEK, mitogen‑activated protein kinase; mTORC1, mechanistic target of rapamycin complex I; p70S6K, p70S6 kinase; PI3K, phosphatidyl inositol-3 kinase; PSD-95, postsynaptic density protein-95; TrKB, tropomyosin receptor kinase B; 4E-BP1, eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1.

    Techniques Used: Protein-Protein interactions, Activation Assay, Derivative Assay, Binding Assay

    Related Articles

    Cell-Signaling:

    Article Title: Establishment of a Depression Model Using Dexamethasone-treated Three-dimensional Cultured Rat Cortical Cells
    Article Snippet: ERK1/2 , Cell signaling Technology (4695) , AB_390779 , WB (1:1,000). .. p-Ser 2448 -mTORC1 , Cell Signaling Technology (2971) , AB_330970 , WB (1:1,000). .. mTORC1 , Cell Signaling Technology (2972) , AB_330978 , WB (1:1,000).

    Western Blot:

    Article Title: Establishment of a Depression Model Using Dexamethasone-treated Three-dimensional Cultured Rat Cortical Cells
    Article Snippet: ERK1/2 , Cell signaling Technology (4695) , AB_390779 , WB (1:1,000). .. p-Ser 2448 -mTORC1 , Cell Signaling Technology (2971) , AB_330970 , WB (1:1,000). .. mTORC1 , Cell Signaling Technology (2972) , AB_330978 , WB (1:1,000).

    other:

    Article Title: Leucine alters hepatic glucose/lipid homeostasis via the myostatin-AMP-activated protein kinase pathway - potential implications for nonalcoholic fatty liver disease
    Article Snippet: Antibodies for mTORC1, p(Ser 2448 )-mTORC1, p(Thr 389 )-p70-S6K1, AMPKα, p(Thr 172 )-AMPKα, AKT and p(Ser 473 )-AKT were from Cell Signaling Technology (Boston, MA, USA) and B-actin antibody was from Santa Cruz Biotechnology (Santa Cruz, CA, USA).



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    p ser 2448 mtorc1  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc p ser 2448 mtorc1
    Changes in the phosphorylation of <t>mTORC1-mediated</t> proteins and in the expression of synaptic proteins after DEX exposure. Beginning on DIV 10, the neural spheroids were exposed to 100 μM DEX for 5 days. Western blotting and immunofluorescence were performed using each primary antibody (n = 4 biological replicates). (A) Western blotting revealed the levels of phospho-Ser 2448 -mTORC1 (a), phospho- Thr 37/46 -4E-BP1 (b), and phospho-Thr 389 -p70S6K (c). (B) Western blot analysis and representative images of immunoblots of PSD-95 (a) and GluA1 (b) are shown. Synaptic markers: PSD-95 (green) costained with the neuronal marker MAP-2 (red); GluA1 (green) costained with MAP-2 (red). Scale bar: 100 μm. The data are presented as the means ± standard deviations. mTORC1, mechanistic target of rapamycin complex I; DEX, dexamethasone; DIV, days in vitro; 4E-BP1, eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1; PSD-95, postsynaptic density protein-95; GluA1, AMPA receptor subunit glutamate receptor 1; MAP-2, microtubule-associated protein-2; CON, controls. * p < 0.05 or ** p < 0.01 vs. CON.
    P Ser 2448 Mtorc1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p+ser+2448+mtorc1/Phospho-mTOR+(Ser2448)+Antibody/pmc12264662-10-0-4
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    p-mtorc1 (ser 2448) antibody  (Cell Signaling Technology Inc)
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    Changes in the phosphorylation of <t>mTORC1-mediated</t> proteins and in the expression of synaptic proteins after DEX exposure. Beginning on DIV 10, the neural spheroids were exposed to 100 μM DEX for 5 days. Western blotting and immunofluorescence were performed using each primary antibody (n = 4 biological replicates). (A) Western blotting revealed the levels of phospho-Ser 2448 -mTORC1 (a), phospho- Thr 37/46 -4E-BP1 (b), and phospho-Thr 389 -p70S6K (c). (B) Western blot analysis and representative images of immunoblots of PSD-95 (a) and GluA1 (b) are shown. Synaptic markers: PSD-95 (green) costained with the neuronal marker MAP-2 (red); GluA1 (green) costained with MAP-2 (red). Scale bar: 100 μm. The data are presented as the means ± standard deviations. mTORC1, mechanistic target of rapamycin complex I; DEX, dexamethasone; DIV, days in vitro; 4E-BP1, eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1; PSD-95, postsynaptic density protein-95; GluA1, AMPA receptor subunit glutamate receptor 1; MAP-2, microtubule-associated protein-2; CON, controls. * p < 0.05 or ** p < 0.01 vs. CON.
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    rabbit polyclonal antibodies against p-mtorc1 (ser 2448)  (Proteintech)
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    Proteintech rabbit polyclonal antibodies against p-mtorc1 (ser 2448)
    Changes in the phosphorylation of <t>mTORC1-mediated</t> proteins and in the expression of synaptic proteins after DEX exposure. Beginning on DIV 10, the neural spheroids were exposed to 100 μM DEX for 5 days. Western blotting and immunofluorescence were performed using each primary antibody (n = 4 biological replicates). (A) Western blotting revealed the levels of phospho-Ser 2448 -mTORC1 (a), phospho- Thr 37/46 -4E-BP1 (b), and phospho-Thr 389 -p70S6K (c). (B) Western blot analysis and representative images of immunoblots of PSD-95 (a) and GluA1 (b) are shown. Synaptic markers: PSD-95 (green) costained with the neuronal marker MAP-2 (red); GluA1 (green) costained with MAP-2 (red). Scale bar: 100 μm. The data are presented as the means ± standard deviations. mTORC1, mechanistic target of rapamycin complex I; DEX, dexamethasone; DIV, days in vitro; 4E-BP1, eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1; PSD-95, postsynaptic density protein-95; GluA1, AMPA receptor subunit glutamate receptor 1; MAP-2, microtubule-associated protein-2; CON, controls. * p < 0.05 or ** p < 0.01 vs. CON.
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    Changes in the phosphorylation of mTORC1-mediated proteins and in the expression of synaptic proteins after DEX exposure. Beginning on DIV 10, the neural spheroids were exposed to 100 μM DEX for 5 days. Western blotting and immunofluorescence were performed using each primary antibody (n = 4 biological replicates). (A) Western blotting revealed the levels of phospho-Ser 2448 -mTORC1 (a), phospho- Thr 37/46 -4E-BP1 (b), and phospho-Thr 389 -p70S6K (c). (B) Western blot analysis and representative images of immunoblots of PSD-95 (a) and GluA1 (b) are shown. Synaptic markers: PSD-95 (green) costained with the neuronal marker MAP-2 (red); GluA1 (green) costained with MAP-2 (red). Scale bar: 100 μm. The data are presented as the means ± standard deviations. mTORC1, mechanistic target of rapamycin complex I; DEX, dexamethasone; DIV, days in vitro; 4E-BP1, eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1; PSD-95, postsynaptic density protein-95; GluA1, AMPA receptor subunit glutamate receptor 1; MAP-2, microtubule-associated protein-2; CON, controls. * p < 0.05 or ** p < 0.01 vs. CON.

    Journal: Clinical Psychopharmacology and Neuroscience

    Article Title: Establishment of a Depression Model Using Dexamethasone-treated Three-dimensional Cultured Rat Cortical Cells

    doi: 10.9758/cpn.25.1269

    Figure Lengend Snippet: Changes in the phosphorylation of mTORC1-mediated proteins and in the expression of synaptic proteins after DEX exposure. Beginning on DIV 10, the neural spheroids were exposed to 100 μM DEX for 5 days. Western blotting and immunofluorescence were performed using each primary antibody (n = 4 biological replicates). (A) Western blotting revealed the levels of phospho-Ser 2448 -mTORC1 (a), phospho- Thr 37/46 -4E-BP1 (b), and phospho-Thr 389 -p70S6K (c). (B) Western blot analysis and representative images of immunoblots of PSD-95 (a) and GluA1 (b) are shown. Synaptic markers: PSD-95 (green) costained with the neuronal marker MAP-2 (red); GluA1 (green) costained with MAP-2 (red). Scale bar: 100 μm. The data are presented as the means ± standard deviations. mTORC1, mechanistic target of rapamycin complex I; DEX, dexamethasone; DIV, days in vitro; 4E-BP1, eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1; PSD-95, postsynaptic density protein-95; GluA1, AMPA receptor subunit glutamate receptor 1; MAP-2, microtubule-associated protein-2; CON, controls. * p < 0.05 or ** p < 0.01 vs. CON.

    Article Snippet: p-Ser 2448 -mTORC1 , Cell Signaling Technology (2971) , AB_330970 , WB (1:1,000).

    Techniques: Phospho-proteomics, Expressing, Western Blot, Immunofluorescence, Marker, In Vitro, Binding Assay

    Schematic diagram showing the molecular mechanisms underlying DEX-induced impaired neuroplasticity. Exposure to DEX downregulates signaling pathways that affect neuroplasticity, including BDNF, sirtuin 1, and mTORC1 signaling. Activation of the mTORC1 signaling pathway induces the synthesis of synaptic proteins as well as BDNF. Secreted BDNF interacts with its receptor TrkB, further activating mTORC1 signaling via PI3K/Akt and MEK/ERK1/2. Therefore, synaptic plasticity is enhanced. Sirtuin 1 is also involved in the regulation of neuroplasticity. The original illustration was created using BioRender (biorender.com). Akt, protein kinase B; AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid; BDNF, brain-derived neurotrophic factor; DEX, dexamethasone; ERK1/2, extracellular signal-regulated kinase 1/2; GluA1, AMPA receptor subunit glutamate receptor 1; MEK, mitogen‑activated protein kinase; mTORC1, mechanistic target of rapamycin complex I; p70S6K, p70S6 kinase; PI3K, phosphatidyl inositol-3 kinase; PSD-95, postsynaptic density protein-95; TrKB, tropomyosin receptor kinase B; 4E-BP1, eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1.

    Journal: Clinical Psychopharmacology and Neuroscience

    Article Title: Establishment of a Depression Model Using Dexamethasone-treated Three-dimensional Cultured Rat Cortical Cells

    doi: 10.9758/cpn.25.1269

    Figure Lengend Snippet: Schematic diagram showing the molecular mechanisms underlying DEX-induced impaired neuroplasticity. Exposure to DEX downregulates signaling pathways that affect neuroplasticity, including BDNF, sirtuin 1, and mTORC1 signaling. Activation of the mTORC1 signaling pathway induces the synthesis of synaptic proteins as well as BDNF. Secreted BDNF interacts with its receptor TrkB, further activating mTORC1 signaling via PI3K/Akt and MEK/ERK1/2. Therefore, synaptic plasticity is enhanced. Sirtuin 1 is also involved in the regulation of neuroplasticity. The original illustration was created using BioRender (biorender.com). Akt, protein kinase B; AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid; BDNF, brain-derived neurotrophic factor; DEX, dexamethasone; ERK1/2, extracellular signal-regulated kinase 1/2; GluA1, AMPA receptor subunit glutamate receptor 1; MEK, mitogen‑activated protein kinase; mTORC1, mechanistic target of rapamycin complex I; p70S6K, p70S6 kinase; PI3K, phosphatidyl inositol-3 kinase; PSD-95, postsynaptic density protein-95; TrKB, tropomyosin receptor kinase B; 4E-BP1, eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1.

    Article Snippet: p-Ser 2448 -mTORC1 , Cell Signaling Technology (2971) , AB_330970 , WB (1:1,000).

    Techniques: Protein-Protein interactions, Activation Assay, Derivative Assay, Binding Assay