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ampk  (Proteintech)


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    Structured Review

    Proteintech ampk
    CMSP <t>reduces</t> <t>AMPK/mTOR</t> pathway activity in ESCC cells. (A) AMP, ATP, and ratio of AMP and ATP response to CMSP treatment in targeted metabolomics. (B) Representative Western blot of p-mTOR, mTOR, p-AMPK, AMPK, p-P70S6K, P70S6K, p-ULK1, and ULK1 following treatment of concentration-dependent CMSP for 36 h. (C) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K, and p-ULK1 following treatment of CMSP (40 μg/ml) for different time. (D) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K and p-ULK1 following treatment of CMSP (40 μg/ml) and rapamycin (20 nM). Data are shown as the mean ± SD ( n = 3); Student’s t test; ** P < 0.01 versus the control group.
    Ampk, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 107 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ampk/product/Proteintech
    Average 95 stars, based on 107 article reviews
    ampk - by Bioz Stars, 2026-03
    95/100 stars

    Images

    1) Product Images from "A Novel Autophagy Inhibitor p -Hydroxylcinnamaldehyde Suppresses Esophageal Squamous Cell Carcinoma by Targeting LDHA Phosphorylation-Mediated Metabolic Reprogramming"

    Article Title: A Novel Autophagy Inhibitor p -Hydroxylcinnamaldehyde Suppresses Esophageal Squamous Cell Carcinoma by Targeting LDHA Phosphorylation-Mediated Metabolic Reprogramming

    Journal: Research

    doi: 10.34133/research.1070

    CMSP reduces AMPK/mTOR pathway activity in ESCC cells. (A) AMP, ATP, and ratio of AMP and ATP response to CMSP treatment in targeted metabolomics. (B) Representative Western blot of p-mTOR, mTOR, p-AMPK, AMPK, p-P70S6K, P70S6K, p-ULK1, and ULK1 following treatment of concentration-dependent CMSP for 36 h. (C) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K, and p-ULK1 following treatment of CMSP (40 μg/ml) for different time. (D) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K and p-ULK1 following treatment of CMSP (40 μg/ml) and rapamycin (20 nM). Data are shown as the mean ± SD ( n = 3); Student’s t test; ** P < 0.01 versus the control group.
    Figure Legend Snippet: CMSP reduces AMPK/mTOR pathway activity in ESCC cells. (A) AMP, ATP, and ratio of AMP and ATP response to CMSP treatment in targeted metabolomics. (B) Representative Western blot of p-mTOR, mTOR, p-AMPK, AMPK, p-P70S6K, P70S6K, p-ULK1, and ULK1 following treatment of concentration-dependent CMSP for 36 h. (C) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K, and p-ULK1 following treatment of CMSP (40 μg/ml) for different time. (D) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K and p-ULK1 following treatment of CMSP (40 μg/ml) and rapamycin (20 nM). Data are shown as the mean ± SD ( n = 3); Student’s t test; ** P < 0.01 versus the control group.

    Techniques Used: Activity Assay, Western Blot, Concentration Assay, Control



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    CMSP <t>reduces</t> <t>AMPK/mTOR</t> pathway activity in ESCC cells. (A) AMP, ATP, and ratio of AMP and ATP response to CMSP treatment in targeted metabolomics. (B) Representative Western blot of p-mTOR, mTOR, p-AMPK, AMPK, p-P70S6K, P70S6K, p-ULK1, and ULK1 following treatment of concentration-dependent CMSP for 36 h. (C) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K, and p-ULK1 following treatment of CMSP (40 μg/ml) for different time. (D) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K and p-ULK1 following treatment of CMSP (40 μg/ml) and rapamycin (20 nM). Data are shown as the mean ± SD ( n = 3); Student’s t test; ** P < 0.01 versus the control group.
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    CMSP <t>reduces</t> <t>AMPK/mTOR</t> pathway activity in ESCC cells. (A) AMP, ATP, and ratio of AMP and ATP response to CMSP treatment in targeted metabolomics. (B) Representative Western blot of p-mTOR, mTOR, p-AMPK, AMPK, p-P70S6K, P70S6K, p-ULK1, and ULK1 following treatment of concentration-dependent CMSP for 36 h. (C) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K, and p-ULK1 following treatment of CMSP (40 μg/ml) for different time. (D) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K and p-ULK1 following treatment of CMSP (40 μg/ml) and rapamycin (20 nM). Data are shown as the mean ± SD ( n = 3); Student’s t test; ** P < 0.01 versus the control group.
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    AYN activated <t>AMPKα</t> pathway in tissues. (A) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in epWAT; (B) Relative band intensity <t>for</t> <t>GLUT4/β‐Actin,</t> CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in epWAT; (C) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in skeletal muscles; (D) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in skeletal muscles. (E) AYN intervention increased p‐AMPKα and CPT‐1α expression in livers; (F) Relative band intensity for CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in livers. ( n = 3, +++ p < 0.001, compared with Normal control group; * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Vehicle control group).
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    AYN activated <t>AMPKα</t> pathway in tissues. (A) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in epWAT; (B) Relative band intensity <t>for</t> <t>GLUT4/β‐Actin,</t> CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in epWAT; (C) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in skeletal muscles; (D) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in skeletal muscles. (E) AYN intervention increased p‐AMPKα and CPT‐1α expression in livers; (F) Relative band intensity for CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in livers. ( n = 3, +++ p < 0.001, compared with Normal control group; * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Vehicle control group).
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    AYN activated <t>AMPKα</t> pathway in tissues. (A) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in epWAT; (B) Relative band intensity <t>for</t> <t>GLUT4/β‐Actin,</t> CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in epWAT; (C) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in skeletal muscles; (D) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in skeletal muscles. (E) AYN intervention increased p‐AMPKα and CPT‐1α expression in livers; (F) Relative band intensity for CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in livers. ( n = 3, +++ p < 0.001, compared with Normal control group; * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Vehicle control group).
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    AYN activated <t>AMPKα</t> pathway in tissues. (A) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in epWAT; (B) Relative band intensity <t>for</t> <t>GLUT4/β‐Actin,</t> CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in epWAT; (C) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in skeletal muscles; (D) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in skeletal muscles. (E) AYN intervention increased p‐AMPKα and CPT‐1α expression in livers; (F) Relative band intensity for CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in livers. ( n = 3, +++ p < 0.001, compared with Normal control group; * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Vehicle control group).
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    AYN activated <t>AMPKα</t> pathway in tissues. (A) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in epWAT; (B) Relative band intensity <t>for</t> <t>GLUT4/β‐Actin,</t> CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in epWAT; (C) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in skeletal muscles; (D) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in skeletal muscles. (E) AYN intervention increased p‐AMPKα and CPT‐1α expression in livers; (F) Relative band intensity for CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in livers. ( n = 3, +++ p < 0.001, compared with Normal control group; * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Vehicle control group).
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    AYN activated <t>AMPKα</t> pathway in tissues. (A) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in epWAT; (B) Relative band intensity <t>for</t> <t>GLUT4/β‐Actin,</t> CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in epWAT; (C) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in skeletal muscles; (D) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in skeletal muscles. (E) AYN intervention increased p‐AMPKα and CPT‐1α expression in livers; (F) Relative band intensity for CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in livers. ( n = 3, +++ p < 0.001, compared with Normal control group; * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Vehicle control group).
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    Image Search Results


    CMSP reduces AMPK/mTOR pathway activity in ESCC cells. (A) AMP, ATP, and ratio of AMP and ATP response to CMSP treatment in targeted metabolomics. (B) Representative Western blot of p-mTOR, mTOR, p-AMPK, AMPK, p-P70S6K, P70S6K, p-ULK1, and ULK1 following treatment of concentration-dependent CMSP for 36 h. (C) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K, and p-ULK1 following treatment of CMSP (40 μg/ml) for different time. (D) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K and p-ULK1 following treatment of CMSP (40 μg/ml) and rapamycin (20 nM). Data are shown as the mean ± SD ( n = 3); Student’s t test; ** P < 0.01 versus the control group.

    Journal: Research

    Article Title: A Novel Autophagy Inhibitor p -Hydroxylcinnamaldehyde Suppresses Esophageal Squamous Cell Carcinoma by Targeting LDHA Phosphorylation-Mediated Metabolic Reprogramming

    doi: 10.34133/research.1070

    Figure Lengend Snippet: CMSP reduces AMPK/mTOR pathway activity in ESCC cells. (A) AMP, ATP, and ratio of AMP and ATP response to CMSP treatment in targeted metabolomics. (B) Representative Western blot of p-mTOR, mTOR, p-AMPK, AMPK, p-P70S6K, P70S6K, p-ULK1, and ULK1 following treatment of concentration-dependent CMSP for 36 h. (C) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K, and p-ULK1 following treatment of CMSP (40 μg/ml) for different time. (D) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K and p-ULK1 following treatment of CMSP (40 μg/ml) and rapamycin (20 nM). Data are shown as the mean ± SD ( n = 3); Student’s t test; ** P < 0.01 versus the control group.

    Article Snippet: Antibodies against actin (20536-1-AP), LC3B (14600-1-AP), glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (10494-1-AP), p-mTOR (67778-1-Ig), mTOR (66888-1-Ig), AMPK (66536-1-Ig), P70S6K (14485-1-AP), and ULK1 (20986-1-AP) were purchased from Proteintech Group (Wuhan, China).

    Techniques: Activity Assay, Western Blot, Concentration Assay, Control

    AYN activated AMPKα pathway in tissues. (A) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in epWAT; (B) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in epWAT; (C) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in skeletal muscles; (D) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in skeletal muscles. (E) AYN intervention increased p‐AMPKα and CPT‐1α expression in livers; (F) Relative band intensity for CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in livers. ( n = 3, +++ p < 0.001, compared with Normal control group; * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Vehicle control group).

    Journal: Food Science & Nutrition

    Article Title: Anti‐Diabetic Effects of Ayanin, a Flavonoid Compound, in STZ / HFD ‐Induced Diabetic Mice by Upregulating GLUT4 and Suppressing Macrophage‐Driven Inflammation in Adipose Tissues

    doi: 10.1002/fsn3.71429

    Figure Lengend Snippet: AYN activated AMPKα pathway in tissues. (A) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in epWAT; (B) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in epWAT; (C) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in skeletal muscles; (D) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in skeletal muscles. (E) AYN intervention increased p‐AMPKα and CPT‐1α expression in livers; (F) Relative band intensity for CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in livers. ( n = 3, +++ p < 0.001, compared with Normal control group; * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Vehicle control group).

    Article Snippet: Antibodies of β‐actin, GLUT4, Cpt‐1α, AMPKα, p‐AMPKα and corresponding secondary antibodies were purchased from Proteintech Group (Wuhan, China).

    Techniques: Expressing, Muscles, Control

    AYN increased glucose uptake of 3T3‐L1 adipocytes by activating AMPKα/GLUT4 pathway. (A) AYN increased GLUT4 and p‐AMPKα expression in 3T3‐L1 adipocytes; (B) Relative band intensity for GLUT4/β‐Actin, p‐AMPKα/AMPKα for protein in 3T3‐L1 adipocytes; (C) AYN increased the glucose uptake of 3T3‐L1 adipocytes; (D) AMPKα inhibitor, Compound C, suppressed the GLUT4 expression of 3T3‐L1 adipocytes induced by AYN; (E) Compound C inhibited the glucose uptake of 3T3‐L1 adipocytes induced by AYN. ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Normal control group; +++ p < 0.001, compared with AYN group in E).

    Journal: Food Science & Nutrition

    Article Title: Anti‐Diabetic Effects of Ayanin, a Flavonoid Compound, in STZ / HFD ‐Induced Diabetic Mice by Upregulating GLUT4 and Suppressing Macrophage‐Driven Inflammation in Adipose Tissues

    doi: 10.1002/fsn3.71429

    Figure Lengend Snippet: AYN increased glucose uptake of 3T3‐L1 adipocytes by activating AMPKα/GLUT4 pathway. (A) AYN increased GLUT4 and p‐AMPKα expression in 3T3‐L1 adipocytes; (B) Relative band intensity for GLUT4/β‐Actin, p‐AMPKα/AMPKα for protein in 3T3‐L1 adipocytes; (C) AYN increased the glucose uptake of 3T3‐L1 adipocytes; (D) AMPKα inhibitor, Compound C, suppressed the GLUT4 expression of 3T3‐L1 adipocytes induced by AYN; (E) Compound C inhibited the glucose uptake of 3T3‐L1 adipocytes induced by AYN. ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Normal control group; +++ p < 0.001, compared with AYN group in E).

    Article Snippet: Antibodies of β‐actin, GLUT4, Cpt‐1α, AMPKα, p‐AMPKα and corresponding secondary antibodies were purchased from Proteintech Group (Wuhan, China).

    Techniques: Expressing, Control