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unc 51 like autophagy  (Proteintech)


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    Proteintech unc 51 like autophagy
    Unc 51 Like Autophagy, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 204 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/unc+51+like+autophagy/ULK1+Antibody/pm40407263-89-46-53
    Average 96 stars, based on 204 article reviews
    unc 51 like autophagy - by Bioz Stars, 2026-10
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    Article Title: Apigenin attenuates the atherosclerotic lesions through enhancing selective autophagy/lipophagy and promoting RCT process
    Article Snippet: The following primary antibodies were used: β-actin (ab8226, 1:2000, Abcam, RRID: AB_3696461, UniProt ID: P60709 ), α-tubulin (ab7291, 1:5000, Abcam, RRID: AB_3696470, UniProt ID: P68366 ), ATP-binding cassette transporter 5 (ABCG5) (27722-1-AP, 1:1000, Proteintech, RRID: AB_2880952, UniProt ID: Q9H222 ), Beclin-1 (66665-1-Ig, 1:2000, Proteintech, RRID: AB_2882020, UniProt ID: Q14457 ), unc-51-like autophagy-activating kinase 1 (ULK1) (20986-1-AP, 1:1000, Proteintech, RRID: AB_2878783, UniProt ID: O75385 ), UVRAG (19571-1-AP, 1:1000, Proteintech, RRID: AB_10640523, UniProt ID: Q9P2Y5 ), LC3 (18725-1-AP, 1:2000, Proteintech, RRID: AB_2137745, UniProt ID: Q9GZQ8 ), autophagy related protein 3 (ATG3) (11262-2-AP, 1:1000, Proteintech, RRID: AB_2059234, UniProt ID: Q9NT62 ), autophagy related protein 5 (ATG5) (10181-2-AP, 1:2000, Proteintech, RRID: AB_2062045, UniProt ID: Q9H1Y0 ), scavenger receptor class B type I (SR-BI) (ab217318, 1:2000, Abcam, RRID: AB_3696478, UniProt ID: Q8WTV0 ).

    Article Title: Apigenin attenuates the atherosclerotic lesions through enhancing selective autophagy/lipophagy and promoting RCT process.
    Article Snippet: The following primary antibodies were used: β-actin (ab8226, 1:2000, Abcam, RRID: AB_3696461, UniProt ID: P60709), α-tubulin (ab7291, 1:5000, Abcam, RRID: AB_3696470, UniProt ID: P68366), ATP-binding cassette transporter 5 (ABCG5) (27722-1-AP, 1:1000, Proteintech, RRID: AB_2880952, UniProt ID: Q9H222), Beclin-1 (66665-1-Ig, 1:2000, Proteintech, RRID: AB_2882020, UniProt ID: Q14457), unc-51-like autophagy-activating kinase 1 (ULK1) (20986-1-AP, 1:1000, Proteintech, RRID: AB_2878783, UniProt ID: O75385), UVRAG (19571-1-AP, 1:1000, Proteintech, RRID: AB_10640523, UniProt ID: Q9P2Y5), LC3 (18725-1-AP, 1:2000, Proteintech, RRID: AB_2137745, UniProt ID: Q9GZQ8), autophagy related protein 3 (ATG3) (11262-2-AP, 1:1000, Proteintech, RRID: AB_2059234, UniProt ID: Q9NT62), autophagy related protein 5 (ATG5) (10181-2-AP, 1:2000, Proteintech, RRID: AB_2062045, UniProt ID: Q9H1Y0), scavenger receptor class B type I (SR-BI) (ab217318, 1:2000, Abcam, RRID: AB_3696478, UniProt ID: Q8WTV0).

    Pyrolysis Gas Chromatography:

    Article Title: CYLD Regulates T Cell Metabolism and Mitochondrial Autophagy through LKB1/AMPKα Pathway
    Article Snippet: The deubiquitinating enzyme cylindromatosis (CYLD) plays a fundamental role in regulating T cell development and activation.. Previous studies have shown that CYLD is associated with autophagy, while AMP activated protein kinase (AMPK) pathway regulates the development of autophagy and affects cell metabolism.. However, the mechanism by which CYLD affects autophagy and whether it affects the downstream metabolism of AMPKα remains unclear.



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    Chaperonin-containing tailless complex polypeptide 1 subunit 6A affects the autophagy pathway in colorectal cancer cells. A and B: Cell lysates were extracted from knockout (KO)-Control (Ctrl) and KO-chaperonin-containing tailless complex polypeptide 1 subunit 6A (CCT6A) HT29 cells, as well as overexpression (OE)-Ctrl and OE-CCT6A SW480 cells, and then subjected to immunoblotting using the indicated antibodies; C: Following treatment with chloroquine diphosphate salt (CQ, 20 μM, hereafter unless otherwise indicated) for 2 hours, immunoblotting was performed with the total proteins extracted from the indicated cells. DDP: Cisplatin; LC3: Light chain 3; mTOR: Mammalian target of rapamycin; <t>Ulk1:</t> Unc-51-like autophagy activating kinase 1.
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    Chaperonin-containing tailless complex polypeptide 1 subunit 6A affects the autophagy pathway in colorectal cancer cells. A and B: Cell lysates were extracted from knockout (KO)-Control (Ctrl) and KO-chaperonin-containing tailless complex polypeptide 1 subunit 6A (CCT6A) HT29 cells, as well as overexpression (OE)-Ctrl and OE-CCT6A SW480 cells, and then subjected to immunoblotting using the indicated antibodies; C: Following treatment with chloroquine diphosphate salt (CQ, 20 μM, hereafter unless otherwise indicated) for 2 hours, immunoblotting was performed with the total proteins extracted from the indicated cells. DDP: Cisplatin; LC3: Light chain 3; mTOR: Mammalian target of rapamycin; <t>Ulk1:</t> Unc-51-like autophagy activating kinase 1.
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    Chaperonin-containing tailless complex polypeptide 1 subunit 6A affects the autophagy pathway in colorectal cancer cells. A and B: Cell lysates were extracted from knockout (KO)-Control (Ctrl) and KO-chaperonin-containing tailless complex polypeptide 1 subunit 6A (CCT6A) HT29 cells, as well as overexpression (OE)-Ctrl and OE-CCT6A SW480 cells, and then subjected to immunoblotting using the indicated antibodies; C: Following treatment with chloroquine diphosphate salt (CQ, 20 μM, hereafter unless otherwise indicated) for 2 hours, immunoblotting was performed with the total proteins extracted from the indicated cells. DDP: Cisplatin; LC3: Light chain 3; mTOR: Mammalian target of rapamycin; <t>Ulk1:</t> Unc-51-like autophagy activating kinase 1.
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    p unc 51 like autophagy activating kinase 1 ulk1  (Cell Signaling Technology Inc)
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    Fig. 6. Icariin mediated autophagy pathways bidirectionally. A. The expression of p-serine/ threonine protein kinase (Akt)/ Akt total, p-mammalian target of rapamycin (mTOR)/mTOR total, p-AMP-activated protein kinase (AMPK)/AMPK total, p-unc- 51-like autophagy activating kinase 1 <t>(ULK1)</t> <t>(Ser555)/ULK1</t> total, and p-ULK (Ser757)/ULK1 total using western blotting; B. Quantification of p-Akt/ Akt total (H = 6.25, p = 0.04); C. Quantification of p-mTOR/ mTOR total (H = 6.25, p = 0.04); D. Quantification of p-AMPK/ AMPK total (H = 6.30, p = 0.04); E. Quantification of p-ULK1 (Ser555)/ULK1 total (H = 6.25, p = 0.04); F. Quantification of p-ULK1 (Ser 757)/ULK1 total (H = 6.25, p = 0.04). The Kruskal– Wallis H test and Dunn’s post hoc test were performed in the B, C, D, E, and F plots. Box bodies represent M (p25, p75), and upper bars and lower bars represent maximum and minimum, respectively (n = 3). The p-AKT/ AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1 were increased, while p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1 were decreased in the model group. Icariin reduced p-AKT/AKT, p-mTOR/ mTOR and p-ULK1 (Ser757)/ULK1, and increased p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1Fig. 6. Icariin mediated autophagy pathways bidirectionally. A. The expression of p-serine/threonine protein kinase (Akt)/Akt total, p-mammalian target of rapamycin (mTOR)/mTOR total, p-AMP-activated protein kinase (AMPK)/AMPK total, p-unc-51-like autophagy activating kinase 1 (ULK1) (Ser555)/ULK1 total, and p-ULK (Ser757)/ULK1 total using western blotting; B. Quantification of p-Akt/Akt total (H = 6.25, p = 0.04); C. Quantification of p-mTOR/mTOR total (H = 6.25, p = 0.04); D. Quantification of p-AMPK/AMPK total (H = 6.30, p = 0.04); E. Quantification of p-ULK1 (Ser555)/ULK1 total (H = 6.25, p = 0.04); F. Quantification of p-ULK1 (Ser 757)/ULK1 total (H = 6.25, p = 0.04). The Kruskal–Wallis H test and Dunn’s post hoc test were performed in the B, C, D, E, and F plots. Box bodies represent M (p25, p75), and upper bars and lower bars represent maximum and minimum, respectively (n = 3). The p-AKT/AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1 were increased, while p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1 were decreased in the model group. Icariin reduced p-AKT/AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1, and increased p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1
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    Fig. 6. Icariin mediated autophagy pathways bidirectionally. A. The expression of p-serine/ threonine protein kinase (Akt)/ Akt total, p-mammalian target of rapamycin (mTOR)/mTOR total, p-AMP-activated protein kinase (AMPK)/AMPK total, p-unc- 51-like autophagy activating kinase 1 <t>(ULK1)</t> <t>(Ser555)/ULK1</t> total, and p-ULK (Ser757)/ULK1 total using western blotting; B. Quantification of p-Akt/ Akt total (H = 6.25, p = 0.04); C. Quantification of p-mTOR/ mTOR total (H = 6.25, p = 0.04); D. Quantification of p-AMPK/ AMPK total (H = 6.30, p = 0.04); E. Quantification of p-ULK1 (Ser555)/ULK1 total (H = 6.25, p = 0.04); F. Quantification of p-ULK1 (Ser 757)/ULK1 total (H = 6.25, p = 0.04). The Kruskal– Wallis H test and Dunn’s post hoc test were performed in the B, C, D, E, and F plots. Box bodies represent M (p25, p75), and upper bars and lower bars represent maximum and minimum, respectively (n = 3). The p-AKT/ AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1 were increased, while p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1 were decreased in the model group. Icariin reduced p-AKT/AKT, p-mTOR/ mTOR and p-ULK1 (Ser757)/ULK1, and increased p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1Fig. 6. Icariin mediated autophagy pathways bidirectionally. A. The expression of p-serine/threonine protein kinase (Akt)/Akt total, p-mammalian target of rapamycin (mTOR)/mTOR total, p-AMP-activated protein kinase (AMPK)/AMPK total, p-unc-51-like autophagy activating kinase 1 (ULK1) (Ser555)/ULK1 total, and p-ULK (Ser757)/ULK1 total using western blotting; B. Quantification of p-Akt/Akt total (H = 6.25, p = 0.04); C. Quantification of p-mTOR/mTOR total (H = 6.25, p = 0.04); D. Quantification of p-AMPK/AMPK total (H = 6.30, p = 0.04); E. Quantification of p-ULK1 (Ser555)/ULK1 total (H = 6.25, p = 0.04); F. Quantification of p-ULK1 (Ser 757)/ULK1 total (H = 6.25, p = 0.04). The Kruskal–Wallis H test and Dunn’s post hoc test were performed in the B, C, D, E, and F plots. Box bodies represent M (p25, p75), and upper bars and lower bars represent maximum and minimum, respectively (n = 3). The p-AKT/AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1 were increased, while p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1 were decreased in the model group. Icariin reduced p-AKT/AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1, and increased p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1
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    Fig. 6. Icariin mediated autophagy pathways bidirectionally. A. The expression of p-serine/ threonine protein kinase (Akt)/ Akt total, p-mammalian target of rapamycin (mTOR)/mTOR total, p-AMP-activated protein kinase (AMPK)/AMPK total, p-unc- 51-like autophagy activating kinase 1 <t>(ULK1)</t> <t>(Ser555)/ULK1</t> total, and p-ULK (Ser757)/ULK1 total using western blotting; B. Quantification of p-Akt/ Akt total (H = 6.25, p = 0.04); C. Quantification of p-mTOR/ mTOR total (H = 6.25, p = 0.04); D. Quantification of p-AMPK/ AMPK total (H = 6.30, p = 0.04); E. Quantification of p-ULK1 (Ser555)/ULK1 total (H = 6.25, p = 0.04); F. Quantification of p-ULK1 (Ser 757)/ULK1 total (H = 6.25, p = 0.04). The Kruskal– Wallis H test and Dunn’s post hoc test were performed in the B, C, D, E, and F plots. Box bodies represent M (p25, p75), and upper bars and lower bars represent maximum and minimum, respectively (n = 3). The p-AKT/ AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1 were increased, while p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1 were decreased in the model group. Icariin reduced p-AKT/AKT, p-mTOR/ mTOR and p-ULK1 (Ser757)/ULK1, and increased p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1Fig. 6. Icariin mediated autophagy pathways bidirectionally. A. The expression of p-serine/threonine protein kinase (Akt)/Akt total, p-mammalian target of rapamycin (mTOR)/mTOR total, p-AMP-activated protein kinase (AMPK)/AMPK total, p-unc-51-like autophagy activating kinase 1 (ULK1) (Ser555)/ULK1 total, and p-ULK (Ser757)/ULK1 total using western blotting; B. Quantification of p-Akt/Akt total (H = 6.25, p = 0.04); C. Quantification of p-mTOR/mTOR total (H = 6.25, p = 0.04); D. Quantification of p-AMPK/AMPK total (H = 6.30, p = 0.04); E. Quantification of p-ULK1 (Ser555)/ULK1 total (H = 6.25, p = 0.04); F. Quantification of p-ULK1 (Ser 757)/ULK1 total (H = 6.25, p = 0.04). The Kruskal–Wallis H test and Dunn’s post hoc test were performed in the B, C, D, E, and F plots. Box bodies represent M (p25, p75), and upper bars and lower bars represent maximum and minimum, respectively (n = 3). The p-AKT/AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1 were increased, while p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1 were decreased in the model group. Icariin reduced p-AKT/AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1, and increased p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1
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    ser555-phosphorylated unc-51-like autophagy activating kinase  (Cell Signaling Technology Inc)
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    Fig. 6. Icariin mediated autophagy pathways bidirectionally. A. The expression of p-serine/ threonine protein kinase (Akt)/ Akt total, p-mammalian target of rapamycin (mTOR)/mTOR total, p-AMP-activated protein kinase (AMPK)/AMPK total, p-unc- 51-like autophagy activating kinase 1 <t>(ULK1)</t> <t>(Ser555)/ULK1</t> total, and p-ULK (Ser757)/ULK1 total using western blotting; B. Quantification of p-Akt/ Akt total (H = 6.25, p = 0.04); C. Quantification of p-mTOR/ mTOR total (H = 6.25, p = 0.04); D. Quantification of p-AMPK/ AMPK total (H = 6.30, p = 0.04); E. Quantification of p-ULK1 (Ser555)/ULK1 total (H = 6.25, p = 0.04); F. Quantification of p-ULK1 (Ser 757)/ULK1 total (H = 6.25, p = 0.04). The Kruskal– Wallis H test and Dunn’s post hoc test were performed in the B, C, D, E, and F plots. Box bodies represent M (p25, p75), and upper bars and lower bars represent maximum and minimum, respectively (n = 3). The p-AKT/ AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1 were increased, while p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1 were decreased in the model group. Icariin reduced p-AKT/AKT, p-mTOR/ mTOR and p-ULK1 (Ser757)/ULK1, and increased p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1Fig. 6. Icariin mediated autophagy pathways bidirectionally. A. The expression of p-serine/threonine protein kinase (Akt)/Akt total, p-mammalian target of rapamycin (mTOR)/mTOR total, p-AMP-activated protein kinase (AMPK)/AMPK total, p-unc-51-like autophagy activating kinase 1 (ULK1) (Ser555)/ULK1 total, and p-ULK (Ser757)/ULK1 total using western blotting; B. Quantification of p-Akt/Akt total (H = 6.25, p = 0.04); C. Quantification of p-mTOR/mTOR total (H = 6.25, p = 0.04); D. Quantification of p-AMPK/AMPK total (H = 6.30, p = 0.04); E. Quantification of p-ULK1 (Ser555)/ULK1 total (H = 6.25, p = 0.04); F. Quantification of p-ULK1 (Ser 757)/ULK1 total (H = 6.25, p = 0.04). The Kruskal–Wallis H test and Dunn’s post hoc test were performed in the B, C, D, E, and F plots. Box bodies represent M (p25, p75), and upper bars and lower bars represent maximum and minimum, respectively (n = 3). The p-AKT/AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1 were increased, while p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1 were decreased in the model group. Icariin reduced p-AKT/AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1, and increased p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1
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    Chaperonin-containing tailless complex polypeptide 1 subunit 6A affects the autophagy pathway in colorectal cancer cells. A and B: Cell lysates were extracted from knockout (KO)-Control (Ctrl) and KO-chaperonin-containing tailless complex polypeptide 1 subunit 6A (CCT6A) HT29 cells, as well as overexpression (OE)-Ctrl and OE-CCT6A SW480 cells, and then subjected to immunoblotting using the indicated antibodies; C: Following treatment with chloroquine diphosphate salt (CQ, 20 μM, hereafter unless otherwise indicated) for 2 hours, immunoblotting was performed with the total proteins extracted from the indicated cells. DDP: Cisplatin; LC3: Light chain 3; mTOR: Mammalian target of rapamycin; Ulk1: Unc-51-like autophagy activating kinase 1.

    Journal: World Journal of Gastroenterology

    Article Title: Chaperonin-containing tailless complex polypeptide 1 subunit 6A negatively regulates autophagy and protects colorectal cancer cells from cisplatin-induced cytotoxicity

    doi: 10.3748/wjg.v31.i18.105729

    Figure Lengend Snippet: Chaperonin-containing tailless complex polypeptide 1 subunit 6A affects the autophagy pathway in colorectal cancer cells. A and B: Cell lysates were extracted from knockout (KO)-Control (Ctrl) and KO-chaperonin-containing tailless complex polypeptide 1 subunit 6A (CCT6A) HT29 cells, as well as overexpression (OE)-Ctrl and OE-CCT6A SW480 cells, and then subjected to immunoblotting using the indicated antibodies; C: Following treatment with chloroquine diphosphate salt (CQ, 20 μM, hereafter unless otherwise indicated) for 2 hours, immunoblotting was performed with the total proteins extracted from the indicated cells. DDP: Cisplatin; LC3: Light chain 3; mTOR: Mammalian target of rapamycin; Ulk1: Unc-51-like autophagy activating kinase 1.

    Article Snippet: Primary antibodies against CCT6A (19793-1-AP), tubulin (66240-1-Ig), phosphorylated Unc-51-like autophagy activating kinase 1 (phospho-Ulk1) (Ser556, 80218-1-RR), Beclin-1 (11306-1-AP), and p62 (66184-1-Ig) were purchased from Proteintech Group (Wuhan, China).

    Techniques: Knock-Out, Control, Over Expression, Western Blot

    Fig. 6. Icariin mediated autophagy pathways bidirectionally. A. The expression of p-serine/ threonine protein kinase (Akt)/ Akt total, p-mammalian target of rapamycin (mTOR)/mTOR total, p-AMP-activated protein kinase (AMPK)/AMPK total, p-unc- 51-like autophagy activating kinase 1 (ULK1) (Ser555)/ULK1 total, and p-ULK (Ser757)/ULK1 total using western blotting; B. Quantification of p-Akt/ Akt total (H = 6.25, p = 0.04); C. Quantification of p-mTOR/ mTOR total (H = 6.25, p = 0.04); D. Quantification of p-AMPK/ AMPK total (H = 6.30, p = 0.04); E. Quantification of p-ULK1 (Ser555)/ULK1 total (H = 6.25, p = 0.04); F. Quantification of p-ULK1 (Ser 757)/ULK1 total (H = 6.25, p = 0.04). The Kruskal– Wallis H test and Dunn’s post hoc test were performed in the B, C, D, E, and F plots. Box bodies represent M (p25, p75), and upper bars and lower bars represent maximum and minimum, respectively (n = 3). The p-AKT/ AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1 were increased, while p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1 were decreased in the model group. Icariin reduced p-AKT/AKT, p-mTOR/ mTOR and p-ULK1 (Ser757)/ULK1, and increased p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1Fig. 6. Icariin mediated autophagy pathways bidirectionally. A. The expression of p-serine/threonine protein kinase (Akt)/Akt total, p-mammalian target of rapamycin (mTOR)/mTOR total, p-AMP-activated protein kinase (AMPK)/AMPK total, p-unc-51-like autophagy activating kinase 1 (ULK1) (Ser555)/ULK1 total, and p-ULK (Ser757)/ULK1 total using western blotting; B. Quantification of p-Akt/Akt total (H = 6.25, p = 0.04); C. Quantification of p-mTOR/mTOR total (H = 6.25, p = 0.04); D. Quantification of p-AMPK/AMPK total (H = 6.30, p = 0.04); E. Quantification of p-ULK1 (Ser555)/ULK1 total (H = 6.25, p = 0.04); F. Quantification of p-ULK1 (Ser 757)/ULK1 total (H = 6.25, p = 0.04). The Kruskal–Wallis H test and Dunn’s post hoc test were performed in the B, C, D, E, and F plots. Box bodies represent M (p25, p75), and upper bars and lower bars represent maximum and minimum, respectively (n = 3). The p-AKT/AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1 were increased, while p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1 were decreased in the model group. Icariin reduced p-AKT/AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1, and increased p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1

    Journal: Advances in clinical and experimental medicine : official organ Wroclaw Medical University

    Article Title: Icariin ameliorates osteoporosis by activating autophagy in ovariectomized rats.

    doi: 10.17219/acem/174078

    Figure Lengend Snippet: Fig. 6. Icariin mediated autophagy pathways bidirectionally. A. The expression of p-serine/ threonine protein kinase (Akt)/ Akt total, p-mammalian target of rapamycin (mTOR)/mTOR total, p-AMP-activated protein kinase (AMPK)/AMPK total, p-unc- 51-like autophagy activating kinase 1 (ULK1) (Ser555)/ULK1 total, and p-ULK (Ser757)/ULK1 total using western blotting; B. Quantification of p-Akt/ Akt total (H = 6.25, p = 0.04); C. Quantification of p-mTOR/ mTOR total (H = 6.25, p = 0.04); D. Quantification of p-AMPK/ AMPK total (H = 6.30, p = 0.04); E. Quantification of p-ULK1 (Ser555)/ULK1 total (H = 6.25, p = 0.04); F. Quantification of p-ULK1 (Ser 757)/ULK1 total (H = 6.25, p = 0.04). The Kruskal– Wallis H test and Dunn’s post hoc test were performed in the B, C, D, E, and F plots. Box bodies represent M (p25, p75), and upper bars and lower bars represent maximum and minimum, respectively (n = 3). The p-AKT/ AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1 were increased, while p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1 were decreased in the model group. Icariin reduced p-AKT/AKT, p-mTOR/ mTOR and p-ULK1 (Ser757)/ULK1, and increased p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1Fig. 6. Icariin mediated autophagy pathways bidirectionally. A. The expression of p-serine/threonine protein kinase (Akt)/Akt total, p-mammalian target of rapamycin (mTOR)/mTOR total, p-AMP-activated protein kinase (AMPK)/AMPK total, p-unc-51-like autophagy activating kinase 1 (ULK1) (Ser555)/ULK1 total, and p-ULK (Ser757)/ULK1 total using western blotting; B. Quantification of p-Akt/Akt total (H = 6.25, p = 0.04); C. Quantification of p-mTOR/mTOR total (H = 6.25, p = 0.04); D. Quantification of p-AMPK/AMPK total (H = 6.30, p = 0.04); E. Quantification of p-ULK1 (Ser555)/ULK1 total (H = 6.25, p = 0.04); F. Quantification of p-ULK1 (Ser 757)/ULK1 total (H = 6.25, p = 0.04). The Kruskal–Wallis H test and Dunn’s post hoc test were performed in the B, C, D, E, and F plots. Box bodies represent M (p25, p75), and upper bars and lower bars represent maximum and minimum, respectively (n = 3). The p-AKT/AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1 were increased, while p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1 were decreased in the model group. Icariin reduced p-AKT/AKT, p-mTOR/mTOR and p-ULK1 (Ser757)/ULK1, and increased p-AMPK/AMPK and p-ULK1 (Ser555)/ULK1

    Article Snippet: Autophagy-related protein 7 (Atg7) (8558), Akt (9272), p-Akt (4058), Beclin1 (3495), mammalian target of rapamycin (mTOR) (2972), p-unc-51-like autophagy activating kinase 1 (ULK1) (Ser555) (5869), p-mTOR (2971), ULK1 (8054), p-ULK1 (Ser757) (14202), and AMPactivated protein kinase (AMPK) (5832) were purchased from Cell Signaling Technology (Danvers, USA).

    Techniques: Expressing, Western Blot