atg5 Search Results


anti atg5 antibody  (Novus Biologicals)
94
Novus Biologicals anti atg5 antibody
TRIM44 promtoes aggregates deaggregation and clearance via autophagy. (a) Cells were treated with MG132 and immunostained with antibodies to ubiquitin (red) and LC3B-II (green). Arrows indicate ubiquitin-positive aggregates that colocalize with LC3B-positive autophagosomes. Scale bars: 10 μm. (b) Confocal images of TRIM44[OE-CON] and TRIM44[OE] U266 cells after treatment with MG132 (0.5 µM) for 16 h followed by a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA. Arrows indicate cells with remaining aggregates. The relative level of remaining aggregates is determinded by quantifying the percentage of cells with remaining aggregates after a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA (10 mM) and normalized to the percentage of cells with aggregates formed by the 16 h MG132 (0.5 µM) treatment in corresponding cells. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. (c) Confocal images of TRIM44[KD-CON] and TRIM44[KD] U266 cells after treatment with MG132 (0.5 µM) for 16 h followed by a 24-h chase period in normal culture media with DMSO (vehicle), or PP242 (10 nM). Arrows indicate cells with remaining aggregates. Scale bars: 10 µm. The relative level of remaining aggregates is determinded by quantifying the percentage of cells with remaining aggregates after a 24-h chase period in normal culture media with DMSO (vehicle), or PP242 (10 nM) and normalized to the percentage of cells with aggregates formed by the 16 h MG132 (0.5 µM) treatment in corresponding cells. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. (d, e) Confocal images of WT or <t>ATG5</t> KO TRIM44[OE-CON] and TRIM44[OE] U266 cells transfected with NC or ATG5 siRNA after treatment with MG132 (0.5 µM) for 16 h. Aggregates (marked by arrows) were identified by staining with the antibody against ubiquitin (d). Scale bars: 10 µm. The status of aggregates after MG132 treatment was quantified in the histogram. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. The protein level of ATG5 and TRIM44 were assayed by western blots (e). (f, g) Confocal images of WT or BECN1 KO TRIM44[OE-CON] and TRIM44[OE] U266 cells were treated with MG132 (0.5 µM) for 16 h. Aggregates (marked by arrows) were identified by staining with the antibody against ubiquitin (f). Scale bars: 10 µm. The status of aggregates after MG132 treatment was quantified in the histogram. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. The protein level of BECN1 and TRIM44 were assayed by western blot (g). (h, i) Confocal images of RPMI-TRIM44[Tet-on] cells treated with or without DOX (1 µg/mL) transfected with NC or ATG5 siRNA after treatment with MG132 (0.5 µM) for 16 h. The status of aggregates after MG132 treatment was quantified in the histogram. Scale bars: 10 µm. The status of aggregates after MG132 treatment was quantified in the histogram. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. The protein level of ATG5 and TRIM44 were assayed by western blots (h). (j) Confocal images of RPMI-TRIM44[Tet-on] cells treated with or without DOX (1 µg/mL) together with MG132 (5 µM) for 16 h followed by a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA. Arrows indicate cells with remaining aggregates. The relative level of remaining aggregates is determinded by quantifying the percentage of cells with remaining aggregates after a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA and normalized to the percentage of cells with aggregates formed by the 16 h MG132 (5 µM) treatment in corresponding cells. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm.
Anti Atg5 Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 94 stars, based on 1 article reviews
anti atg5 antibody - by Bioz Stars, 2026-04
94/100 stars
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anti atg5  (Novus Biologicals)
93
Novus Biologicals anti atg5
TRIM44 promtoes aggregates deaggregation and clearance via autophagy. (a) Cells were treated with MG132 and immunostained with antibodies to ubiquitin (red) and LC3B-II (green). Arrows indicate ubiquitin-positive aggregates that colocalize with LC3B-positive autophagosomes. Scale bars: 10 μm. (b) Confocal images of TRIM44[OE-CON] and TRIM44[OE] U266 cells after treatment with MG132 (0.5 µM) for 16 h followed by a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA. Arrows indicate cells with remaining aggregates. The relative level of remaining aggregates is determinded by quantifying the percentage of cells with remaining aggregates after a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA (10 mM) and normalized to the percentage of cells with aggregates formed by the 16 h MG132 (0.5 µM) treatment in corresponding cells. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. (c) Confocal images of TRIM44[KD-CON] and TRIM44[KD] U266 cells after treatment with MG132 (0.5 µM) for 16 h followed by a 24-h chase period in normal culture media with DMSO (vehicle), or PP242 (10 nM). Arrows indicate cells with remaining aggregates. Scale bars: 10 µm. The relative level of remaining aggregates is determinded by quantifying the percentage of cells with remaining aggregates after a 24-h chase period in normal culture media with DMSO (vehicle), or PP242 (10 nM) and normalized to the percentage of cells with aggregates formed by the 16 h MG132 (0.5 µM) treatment in corresponding cells. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. (d, e) Confocal images of WT or <t>ATG5</t> KO TRIM44[OE-CON] and TRIM44[OE] U266 cells transfected with NC or ATG5 siRNA after treatment with MG132 (0.5 µM) for 16 h. Aggregates (marked by arrows) were identified by staining with the antibody against ubiquitin (d). Scale bars: 10 µm. The status of aggregates after MG132 treatment was quantified in the histogram. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. The protein level of ATG5 and TRIM44 were assayed by western blots (e). (f, g) Confocal images of WT or BECN1 KO TRIM44[OE-CON] and TRIM44[OE] U266 cells were treated with MG132 (0.5 µM) for 16 h. Aggregates (marked by arrows) were identified by staining with the antibody against ubiquitin (f). Scale bars: 10 µm. The status of aggregates after MG132 treatment was quantified in the histogram. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. The protein level of BECN1 and TRIM44 were assayed by western blot (g). (h, i) Confocal images of RPMI-TRIM44[Tet-on] cells treated with or without DOX (1 µg/mL) transfected with NC or ATG5 siRNA after treatment with MG132 (0.5 µM) for 16 h. The status of aggregates after MG132 treatment was quantified in the histogram. Scale bars: 10 µm. The status of aggregates after MG132 treatment was quantified in the histogram. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. The protein level of ATG5 and TRIM44 were assayed by western blots (h). (j) Confocal images of RPMI-TRIM44[Tet-on] cells treated with or without DOX (1 µg/mL) together with MG132 (5 µM) for 16 h followed by a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA. Arrows indicate cells with remaining aggregates. The relative level of remaining aggregates is determinded by quantifying the percentage of cells with remaining aggregates after a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA and normalized to the percentage of cells with aggregates formed by the 16 h MG132 (5 µM) treatment in corresponding cells. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm.
Anti Atg5, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti atg5/product/Novus Biologicals
Average 93 stars, based on 1 article reviews
anti atg5 - by Bioz Stars, 2026-04
93/100 stars
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mouse anti atg5  (R&D Systems)
90
R&D Systems mouse anti atg5
TRIM44 promtoes aggregates deaggregation and clearance via autophagy. (a) Cells were treated with MG132 and immunostained with antibodies to ubiquitin (red) and LC3B-II (green). Arrows indicate ubiquitin-positive aggregates that colocalize with LC3B-positive autophagosomes. Scale bars: 10 μm. (b) Confocal images of TRIM44[OE-CON] and TRIM44[OE] U266 cells after treatment with MG132 (0.5 µM) for 16 h followed by a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA. Arrows indicate cells with remaining aggregates. The relative level of remaining aggregates is determinded by quantifying the percentage of cells with remaining aggregates after a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA (10 mM) and normalized to the percentage of cells with aggregates formed by the 16 h MG132 (0.5 µM) treatment in corresponding cells. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. (c) Confocal images of TRIM44[KD-CON] and TRIM44[KD] U266 cells after treatment with MG132 (0.5 µM) for 16 h followed by a 24-h chase period in normal culture media with DMSO (vehicle), or PP242 (10 nM). Arrows indicate cells with remaining aggregates. Scale bars: 10 µm. The relative level of remaining aggregates is determinded by quantifying the percentage of cells with remaining aggregates after a 24-h chase period in normal culture media with DMSO (vehicle), or PP242 (10 nM) and normalized to the percentage of cells with aggregates formed by the 16 h MG132 (0.5 µM) treatment in corresponding cells. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. (d, e) Confocal images of WT or <t>ATG5</t> KO TRIM44[OE-CON] and TRIM44[OE] U266 cells transfected with NC or ATG5 siRNA after treatment with MG132 (0.5 µM) for 16 h. Aggregates (marked by arrows) were identified by staining with the antibody against ubiquitin (d). Scale bars: 10 µm. The status of aggregates after MG132 treatment was quantified in the histogram. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. The protein level of ATG5 and TRIM44 were assayed by western blots (e). (f, g) Confocal images of WT or BECN1 KO TRIM44[OE-CON] and TRIM44[OE] U266 cells were treated with MG132 (0.5 µM) for 16 h. Aggregates (marked by arrows) were identified by staining with the antibody against ubiquitin (f). Scale bars: 10 µm. The status of aggregates after MG132 treatment was quantified in the histogram. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. The protein level of BECN1 and TRIM44 were assayed by western blot (g). (h, i) Confocal images of RPMI-TRIM44[Tet-on] cells treated with or without DOX (1 µg/mL) transfected with NC or ATG5 siRNA after treatment with MG132 (0.5 µM) for 16 h. The status of aggregates after MG132 treatment was quantified in the histogram. Scale bars: 10 µm. The status of aggregates after MG132 treatment was quantified in the histogram. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. The protein level of ATG5 and TRIM44 were assayed by western blots (h). (j) Confocal images of RPMI-TRIM44[Tet-on] cells treated with or without DOX (1 µg/mL) together with MG132 (5 µM) for 16 h followed by a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA. Arrows indicate cells with remaining aggregates. The relative level of remaining aggregates is determinded by quantifying the percentage of cells with remaining aggregates after a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA and normalized to the percentage of cells with aggregates formed by the 16 h MG132 (5 µM) treatment in corresponding cells. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm.
Mouse Anti Atg5, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
mouse anti atg5 - by Bioz Stars, 2026-04
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atg5  (Novus Biologicals)
95
Novus Biologicals atg5
The role of autophagy in morphine-mediated synaptic alterations. Representative Western blot (A) and quantification of autophagy mediators (Beclin1, <t>ATG5,</t> p62, and LC3-II; B) in the hippocampal lysates from mouse injected with saline or morphine ( n = 3 to 4/group). *, P < 0.05; **, P < 0.01 versus saline group using Student’s t test. Representative time course Western blot (C) and quantification of LC3-II (D) in primary neurons exposed to morphine. Representative Western blot (E) and quantification of Beclin1, ATG5, p62, and LC3-II (F) in the cell lysates from neurons pretreated with naltrexone for 1 h followed by 24-h morphine treatment. Representative confocal images (G) and quantification of GFP-LC3 puncta (H) of primary hippocampal neurons expressing GFP-LC3 exposed to morphine for 24 h. Bar, 10 µm. **, P < 0.01 versus saline group using Student's t test. Representative Western blot (I) and quantification of LC3-II (J) in the cell lysates of neurons treated with bafilomycin for 4 h after 24-h exposure to morphine. Representative confocal images of GFP-expressing primary rat hippocampal neurons treated with wortmannin (500 µM) for 1 h followed by morphine exposure for 24 h and stained with vGlut1 and GAD65 (K) and quantifications of spine density and excitatory and inhibitory synapses (L). Bar, 5 µm. Representative confocal images of neurons expressing PGK-GFP-scramble or PGK-GFP-shATG7 vector in the presence or absence of morphine for 24 h and stained with vGlut1 and GAD65 (M) and quantifications of spine density and excitatory and inhibitory synapses (N). Bar, 5 µm. Quantification of Western blot results were all normalized to β-actin. Each set of in vitro results was quantified upon four independent experiments. All data are presented as mean ± SD. *, P < 0.05; **, P < 0.01 versus control group; # , P < 0.05; ## , P < 0.01 versus morphine group using one-way ANOVA with post hoc test (except B and H).
Atg5, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/atg5/product/Novus Biologicals
Average 95 stars, based on 1 article reviews
atg5 - by Bioz Stars, 2026-04
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atg5  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc atg5
RT-qPCR validation of hub gene expression following autophagy modulation and photodynamic therapy (PDT). RT-qPCR analysis showing relative mRNA expression levels of autophagy-related hub genes (AKT1, BCL2, BECN1, <t>ATG5)</t> in NPC cell lines (C666-1 and HONE1) under different conditions: control, PDT alone, autophagy activation (rapamycin + PDT), and autophagy inhibition (chloroquine + PDT). Autophagy activation amplified the transcriptional induction of BECN1 and ATG5, whereas inhibition suppressed their expression, indicating that autophagy promotes survival signaling during PDT stress. P -value < 0.05
Atg5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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atg5 rabbit monoclonal antibody  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc atg5 rabbit monoclonal antibody
RT-qPCR validation of hub gene expression following autophagy modulation and photodynamic therapy (PDT). RT-qPCR analysis showing relative mRNA expression levels of autophagy-related hub genes (AKT1, BCL2, BECN1, <t>ATG5)</t> in NPC cell lines (C666-1 and HONE1) under different conditions: control, PDT alone, autophagy activation (rapamycin + PDT), and autophagy inhibition (chloroquine + PDT). Autophagy activation amplified the transcriptional induction of BECN1 and ATG5, whereas inhibition suppressed their expression, indicating that autophagy promotes survival signaling during PDT stress. P -value < 0.05
Atg5 Rabbit Monoclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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atg5 double nickase plasmids h m  (Santa Cruz Biotechnology)
92
Santa Cruz Biotechnology atg5 double nickase plasmids h m
RT-qPCR validation of hub gene expression following autophagy modulation and photodynamic therapy (PDT). RT-qPCR analysis showing relative mRNA expression levels of autophagy-related hub genes (AKT1, BCL2, BECN1, <t>ATG5)</t> in NPC cell lines (C666-1 and HONE1) under different conditions: control, PDT alone, autophagy activation (rapamycin + PDT), and autophagy inhibition (chloroquine + PDT). Autophagy activation amplified the transcriptional induction of BECN1 and ATG5, whereas inhibition suppressed their expression, indicating that autophagy promotes survival signaling during PDT stress. P -value < 0.05
Atg5 Double Nickase Plasmids H M, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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polyclonal antibodies against atg5  (Novus Biologicals)
93
Novus Biologicals polyclonal antibodies against atg5
Figure 1 M. hyopneumoniae infection increases the formation of autophagosome-like vesicles and the expression of autophagy-related proteins in porcine alveolar macrophages. A Autophagosome-like vesicles (arrows) were observed in M. hyopneumoniae-negative (a) and M. hyopneumoniae-positive (b) PAMs by TEM. Ten M. hyopneumoniae-negative and 10 M. hyopneumoniae-positive PAMs were assessed. B Autophagosome-like vesicles (arrows) were observed in mock-infected (a) or AH-infected (b) 3D4/21 cells by TEM. Ten uninfected and 10 AH-infected 3D4/21 cells were assessed. C Results of Western blotting showing the expression of autophagy-related proteins (LC3-II, <t>Atg5,</t> Atg12-Atg5, and Beclin 1) and Mhp366 in 30 M. hyopneumoniae-positive and 10 M. hyopneumoniae-negative PAMs collected from pigs. D Results of Western blotting showing the expression of autophagy-related proteins (LC3-II, Atg5, Atg12-Atg5, and Beclin 1) and P97 protein in 3D4/21 cells after mock infection or AH infection. Mean values from 3 independent experiments are presented. Between-group differences were assessed using a t test; *p ≤ 0.05, **p ≤ 0.01.
Polyclonal Antibodies Against Atg5, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 1 article reviews
polyclonal antibodies against atg5 - by Bioz Stars, 2026-04
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pcmv myc atg5  (Addgene inc)
93
Addgene inc pcmv myc atg5
Figure 1 M. hyopneumoniae infection increases the formation of autophagosome-like vesicles and the expression of autophagy-related proteins in porcine alveolar macrophages. A Autophagosome-like vesicles (arrows) were observed in M. hyopneumoniae-negative (a) and M. hyopneumoniae-positive (b) PAMs by TEM. Ten M. hyopneumoniae-negative and 10 M. hyopneumoniae-positive PAMs were assessed. B Autophagosome-like vesicles (arrows) were observed in mock-infected (a) or AH-infected (b) 3D4/21 cells by TEM. Ten uninfected and 10 AH-infected 3D4/21 cells were assessed. C Results of Western blotting showing the expression of autophagy-related proteins (LC3-II, <t>Atg5,</t> Atg12-Atg5, and Beclin 1) and Mhp366 in 30 M. hyopneumoniae-positive and 10 M. hyopneumoniae-negative PAMs collected from pigs. D Results of Western blotting showing the expression of autophagy-related proteins (LC3-II, Atg5, Atg12-Atg5, and Beclin 1) and P97 protein in 3D4/21 cells after mock infection or AH infection. Mean values from 3 independent experiments are presented. Between-group differences were assessed using a t test; *p ≤ 0.05, **p ≤ 0.01.
Pcmv Myc Atg5, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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matg5  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology matg5
Figure 1 M. hyopneumoniae infection increases the formation of autophagosome-like vesicles and the expression of autophagy-related proteins in porcine alveolar macrophages. A Autophagosome-like vesicles (arrows) were observed in M. hyopneumoniae-negative (a) and M. hyopneumoniae-positive (b) PAMs by TEM. Ten M. hyopneumoniae-negative and 10 M. hyopneumoniae-positive PAMs were assessed. B Autophagosome-like vesicles (arrows) were observed in mock-infected (a) or AH-infected (b) 3D4/21 cells by TEM. Ten uninfected and 10 AH-infected 3D4/21 cells were assessed. C Results of Western blotting showing the expression of autophagy-related proteins (LC3-II, <t>Atg5,</t> Atg12-Atg5, and Beclin 1) and Mhp366 in 30 M. hyopneumoniae-positive and 10 M. hyopneumoniae-negative PAMs collected from pigs. D Results of Western blotting showing the expression of autophagy-related proteins (LC3-II, Atg5, Atg12-Atg5, and Beclin 1) and P97 protein in 3D4/21 cells after mock infection or AH infection. Mean values from 3 independent experiments are presented. Between-group differences were assessed using a t test; *p ≤ 0.05, **p ≤ 0.01.
Matg5, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 1 article reviews
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atg5  (Santa Cruz Biotechnology)
96
Santa Cruz Biotechnology atg5
Figure 1 M. hyopneumoniae infection increases the formation of autophagosome-like vesicles and the expression of autophagy-related proteins in porcine alveolar macrophages. A Autophagosome-like vesicles (arrows) were observed in M. hyopneumoniae-negative (a) and M. hyopneumoniae-positive (b) PAMs by TEM. Ten M. hyopneumoniae-negative and 10 M. hyopneumoniae-positive PAMs were assessed. B Autophagosome-like vesicles (arrows) were observed in mock-infected (a) or AH-infected (b) 3D4/21 cells by TEM. Ten uninfected and 10 AH-infected 3D4/21 cells were assessed. C Results of Western blotting showing the expression of autophagy-related proteins (LC3-II, <t>Atg5,</t> Atg12-Atg5, and Beclin 1) and Mhp366 in 30 M. hyopneumoniae-positive and 10 M. hyopneumoniae-negative PAMs collected from pigs. D Results of Western blotting showing the expression of autophagy-related proteins (LC3-II, Atg5, Atg12-Atg5, and Beclin 1) and P97 protein in 3D4/21 cells after mock infection or AH infection. Mean values from 3 independent experiments are presented. Between-group differences were assessed using a t test; *p ≤ 0.05, **p ≤ 0.01.
Atg5, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mouse anti atg5 primary antibody ac epted manuscriptarticle in press ar tic le in pr es s ac ce pt ed m  (Proteintech)
96
Proteintech mouse anti atg5 primary antibody ac epted manuscriptarticle in press ar tic le in pr es s ac ce pt ed m
Figure 1 M. hyopneumoniae infection increases the formation of autophagosome-like vesicles and the expression of autophagy-related proteins in porcine alveolar macrophages. A Autophagosome-like vesicles (arrows) were observed in M. hyopneumoniae-negative (a) and M. hyopneumoniae-positive (b) PAMs by TEM. Ten M. hyopneumoniae-negative and 10 M. hyopneumoniae-positive PAMs were assessed. B Autophagosome-like vesicles (arrows) were observed in mock-infected (a) or AH-infected (b) 3D4/21 cells by TEM. Ten uninfected and 10 AH-infected 3D4/21 cells were assessed. C Results of Western blotting showing the expression of autophagy-related proteins (LC3-II, <t>Atg5,</t> Atg12-Atg5, and Beclin 1) and Mhp366 in 30 M. hyopneumoniae-positive and 10 M. hyopneumoniae-negative PAMs collected from pigs. D Results of Western blotting showing the expression of autophagy-related proteins (LC3-II, Atg5, Atg12-Atg5, and Beclin 1) and P97 protein in 3D4/21 cells after mock infection or AH infection. Mean values from 3 independent experiments are presented. Between-group differences were assessed using a t test; *p ≤ 0.05, **p ≤ 0.01.
Mouse Anti Atg5 Primary Antibody Ac Epted Manuscriptarticle In Press Ar Tic Le In Pr Es S Ac Ce Pt Ed M, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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TRIM44 promtoes aggregates deaggregation and clearance via autophagy. (a) Cells were treated with MG132 and immunostained with antibodies to ubiquitin (red) and LC3B-II (green). Arrows indicate ubiquitin-positive aggregates that colocalize with LC3B-positive autophagosomes. Scale bars: 10 μm. (b) Confocal images of TRIM44[OE-CON] and TRIM44[OE] U266 cells after treatment with MG132 (0.5 µM) for 16 h followed by a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA. Arrows indicate cells with remaining aggregates. The relative level of remaining aggregates is determinded by quantifying the percentage of cells with remaining aggregates after a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA (10 mM) and normalized to the percentage of cells with aggregates formed by the 16 h MG132 (0.5 µM) treatment in corresponding cells. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. (c) Confocal images of TRIM44[KD-CON] and TRIM44[KD] U266 cells after treatment with MG132 (0.5 µM) for 16 h followed by a 24-h chase period in normal culture media with DMSO (vehicle), or PP242 (10 nM). Arrows indicate cells with remaining aggregates. Scale bars: 10 µm. The relative level of remaining aggregates is determinded by quantifying the percentage of cells with remaining aggregates after a 24-h chase period in normal culture media with DMSO (vehicle), or PP242 (10 nM) and normalized to the percentage of cells with aggregates formed by the 16 h MG132 (0.5 µM) treatment in corresponding cells. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. (d, e) Confocal images of WT or ATG5 KO TRIM44[OE-CON] and TRIM44[OE] U266 cells transfected with NC or ATG5 siRNA after treatment with MG132 (0.5 µM) for 16 h. Aggregates (marked by arrows) were identified by staining with the antibody against ubiquitin (d). Scale bars: 10 µm. The status of aggregates after MG132 treatment was quantified in the histogram. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. The protein level of ATG5 and TRIM44 were assayed by western blots (e). (f, g) Confocal images of WT or BECN1 KO TRIM44[OE-CON] and TRIM44[OE] U266 cells were treated with MG132 (0.5 µM) for 16 h. Aggregates (marked by arrows) were identified by staining with the antibody against ubiquitin (f). Scale bars: 10 µm. The status of aggregates after MG132 treatment was quantified in the histogram. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. The protein level of BECN1 and TRIM44 were assayed by western blot (g). (h, i) Confocal images of RPMI-TRIM44[Tet-on] cells treated with or without DOX (1 µg/mL) transfected with NC or ATG5 siRNA after treatment with MG132 (0.5 µM) for 16 h. The status of aggregates after MG132 treatment was quantified in the histogram. Scale bars: 10 µm. The status of aggregates after MG132 treatment was quantified in the histogram. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. The protein level of ATG5 and TRIM44 were assayed by western blots (h). (j) Confocal images of RPMI-TRIM44[Tet-on] cells treated with or without DOX (1 µg/mL) together with MG132 (5 µM) for 16 h followed by a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA. Arrows indicate cells with remaining aggregates. The relative level of remaining aggregates is determinded by quantifying the percentage of cells with remaining aggregates after a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA and normalized to the percentage of cells with aggregates formed by the 16 h MG132 (5 µM) treatment in corresponding cells. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm.

Journal: Autophagy

Article Title: TRIM44 links the UPS to SQSTM1/p62-dependent aggrephagy and removing misfolded proteins

doi: 10.1080/15548627.2021.1956105

Figure Lengend Snippet: TRIM44 promtoes aggregates deaggregation and clearance via autophagy. (a) Cells were treated with MG132 and immunostained with antibodies to ubiquitin (red) and LC3B-II (green). Arrows indicate ubiquitin-positive aggregates that colocalize with LC3B-positive autophagosomes. Scale bars: 10 μm. (b) Confocal images of TRIM44[OE-CON] and TRIM44[OE] U266 cells after treatment with MG132 (0.5 µM) for 16 h followed by a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA. Arrows indicate cells with remaining aggregates. The relative level of remaining aggregates is determinded by quantifying the percentage of cells with remaining aggregates after a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA (10 mM) and normalized to the percentage of cells with aggregates formed by the 16 h MG132 (0.5 µM) treatment in corresponding cells. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. (c) Confocal images of TRIM44[KD-CON] and TRIM44[KD] U266 cells after treatment with MG132 (0.5 µM) for 16 h followed by a 24-h chase period in normal culture media with DMSO (vehicle), or PP242 (10 nM). Arrows indicate cells with remaining aggregates. Scale bars: 10 µm. The relative level of remaining aggregates is determinded by quantifying the percentage of cells with remaining aggregates after a 24-h chase period in normal culture media with DMSO (vehicle), or PP242 (10 nM) and normalized to the percentage of cells with aggregates formed by the 16 h MG132 (0.5 µM) treatment in corresponding cells. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. (d, e) Confocal images of WT or ATG5 KO TRIM44[OE-CON] and TRIM44[OE] U266 cells transfected with NC or ATG5 siRNA after treatment with MG132 (0.5 µM) for 16 h. Aggregates (marked by arrows) were identified by staining with the antibody against ubiquitin (d). Scale bars: 10 µm. The status of aggregates after MG132 treatment was quantified in the histogram. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. The protein level of ATG5 and TRIM44 were assayed by western blots (e). (f, g) Confocal images of WT or BECN1 KO TRIM44[OE-CON] and TRIM44[OE] U266 cells were treated with MG132 (0.5 µM) for 16 h. Aggregates (marked by arrows) were identified by staining with the antibody against ubiquitin (f). Scale bars: 10 µm. The status of aggregates after MG132 treatment was quantified in the histogram. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. The protein level of BECN1 and TRIM44 were assayed by western blot (g). (h, i) Confocal images of RPMI-TRIM44[Tet-on] cells treated with or without DOX (1 µg/mL) transfected with NC or ATG5 siRNA after treatment with MG132 (0.5 µM) for 16 h. The status of aggregates after MG132 treatment was quantified in the histogram. Scale bars: 10 µm. The status of aggregates after MG132 treatment was quantified in the histogram. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm. The protein level of ATG5 and TRIM44 were assayed by western blots (h). (j) Confocal images of RPMI-TRIM44[Tet-on] cells treated with or without DOX (1 µg/mL) together with MG132 (5 µM) for 16 h followed by a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA. Arrows indicate cells with remaining aggregates. The relative level of remaining aggregates is determinded by quantifying the percentage of cells with remaining aggregates after a 24-h chase period in normal culture media with DMSO (vehicle), or 3-MA and normalized to the percentage of cells with aggregates formed by the 16 h MG132 (5 µM) treatment in corresponding cells. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Scale bars: 10 μm.

Article Snippet: Anti-TRIM44 polyclonal antibody (Proteintech Group, 11,511-1-AP); anti-Ub antibody (Biolegend, 646,301); anti-mCherry antibody (ThermoFisher, PA5-34,974); anti-VIM antibody (ThermoFisher, MA5-11,883); anti-NFE2L2/NRF2 antibody (ThermoFisher, PA5-27,882); anti-20S proteasome antibody (MilliporeSigma, ST1049); anti-TUBG/γ-Tubulin antibody (MilliporeSigma, T5326); anti-ATG5 antibody (Novus Biologicals, NBP2-24,389); Anti-GFP antibody (Santa Cruz Biotechnology, sc-9996); anti-ACTB/β-Actin antibody (Santa Cruz Biotechnology, sc-47,778), anti-HA antibody (Santa Cruz Biotechnology, sc-805); anti-BECN1 antibody (Cell Signaling Technology, 4122); anti-HDAC6 antibody (Cell Signaling Technology, 7558); anti-LC3B antibody (Cell Signaling Technology, 3868); anti-SQSTM1/p62 antibody (Cell Signaling Technology, 88,588); anti-cleaved PARP antibody (Cell Signaling Technology, 5625); Alexa Fluor 594 donkey anti rabbit IgG(H + L) (Invitrogen, A21207); Alexa Fluor 546 goat anti mouse IgG(H + L) (Invitrogen, A11003).

Techniques: Ubiquitin Proteomics, Transfection, Staining, Western Blot

The role of autophagy in morphine-mediated synaptic alterations. Representative Western blot (A) and quantification of autophagy mediators (Beclin1, ATG5, p62, and LC3-II; B) in the hippocampal lysates from mouse injected with saline or morphine ( n = 3 to 4/group). *, P < 0.05; **, P < 0.01 versus saline group using Student’s t test. Representative time course Western blot (C) and quantification of LC3-II (D) in primary neurons exposed to morphine. Representative Western blot (E) and quantification of Beclin1, ATG5, p62, and LC3-II (F) in the cell lysates from neurons pretreated with naltrexone for 1 h followed by 24-h morphine treatment. Representative confocal images (G) and quantification of GFP-LC3 puncta (H) of primary hippocampal neurons expressing GFP-LC3 exposed to morphine for 24 h. Bar, 10 µm. **, P < 0.01 versus saline group using Student's t test. Representative Western blot (I) and quantification of LC3-II (J) in the cell lysates of neurons treated with bafilomycin for 4 h after 24-h exposure to morphine. Representative confocal images of GFP-expressing primary rat hippocampal neurons treated with wortmannin (500 µM) for 1 h followed by morphine exposure for 24 h and stained with vGlut1 and GAD65 (K) and quantifications of spine density and excitatory and inhibitory synapses (L). Bar, 5 µm. Representative confocal images of neurons expressing PGK-GFP-scramble or PGK-GFP-shATG7 vector in the presence or absence of morphine for 24 h and stained with vGlut1 and GAD65 (M) and quantifications of spine density and excitatory and inhibitory synapses (N). Bar, 5 µm. Quantification of Western blot results were all normalized to β-actin. Each set of in vitro results was quantified upon four independent experiments. All data are presented as mean ± SD. *, P < 0.05; **, P < 0.01 versus control group; # , P < 0.05; ## , P < 0.01 versus morphine group using one-way ANOVA with post hoc test (except B and H).

Journal: The Journal of Cell Biology

Article Title: Regulation of morphine-induced synaptic alterations: Role of oxidative stress, ER stress, and autophagy

doi: 10.1083/jcb.201605065

Figure Lengend Snippet: The role of autophagy in morphine-mediated synaptic alterations. Representative Western blot (A) and quantification of autophagy mediators (Beclin1, ATG5, p62, and LC3-II; B) in the hippocampal lysates from mouse injected with saline or morphine ( n = 3 to 4/group). *, P < 0.05; **, P < 0.01 versus saline group using Student’s t test. Representative time course Western blot (C) and quantification of LC3-II (D) in primary neurons exposed to morphine. Representative Western blot (E) and quantification of Beclin1, ATG5, p62, and LC3-II (F) in the cell lysates from neurons pretreated with naltrexone for 1 h followed by 24-h morphine treatment. Representative confocal images (G) and quantification of GFP-LC3 puncta (H) of primary hippocampal neurons expressing GFP-LC3 exposed to morphine for 24 h. Bar, 10 µm. **, P < 0.01 versus saline group using Student's t test. Representative Western blot (I) and quantification of LC3-II (J) in the cell lysates of neurons treated with bafilomycin for 4 h after 24-h exposure to morphine. Representative confocal images of GFP-expressing primary rat hippocampal neurons treated with wortmannin (500 µM) for 1 h followed by morphine exposure for 24 h and stained with vGlut1 and GAD65 (K) and quantifications of spine density and excitatory and inhibitory synapses (L). Bar, 5 µm. Representative confocal images of neurons expressing PGK-GFP-scramble or PGK-GFP-shATG7 vector in the presence or absence of morphine for 24 h and stained with vGlut1 and GAD65 (M) and quantifications of spine density and excitatory and inhibitory synapses (N). Bar, 5 µm. Quantification of Western blot results were all normalized to β-actin. Each set of in vitro results was quantified upon four independent experiments. All data are presented as mean ± SD. *, P < 0.05; **, P < 0.01 versus control group; # , P < 0.05; ## , P < 0.01 versus morphine group using one-way ANOVA with post hoc test (except B and H).

Article Snippet: The Western blots were then probed with respective antibodies recognizing the vGlut1 (1:5,000; catalog no. AB5905, lot no. RRID:AB_2301751; EMD Millipore), PSD95 (1:1,000; catalog no. ab18258; lot no. RRID:AB_444362; Abcam), GAD65 (1:1,000; catalog no. NBP1-33284, lot no. RRID:AB_10004060; Novus Biologicals), gephyrin (1:250; catalog no. 610584, lot no. RRID:AB_397929; BD), BIP (1:1,000; catalog no. 610978, lot no. RRID:AB_398291; BD), pPERK (1:250; catalog no. sc-32577, lot no. RRID:AB_2293243; Santa Cruz Biotechnology, Inc.), PERK (1:250; catalog no. sc-13073, lot no. RRID:AB_2230863; Santa Cruz Biotechnology, Inc.), IRE1α (1:500; catalog no. sc-20790, lot no. RRID:AB_2098712; Santa Cruz Biotechnology, Inc.), ATF6 (1:1,000; catalog no. ab37149, lot no. RRID:AB_725571; Abcam), Beclin1 (1:1,000; catalog no. sc-11427, lot no. RRID:AB_2064465; Santa Cruz Biotechnology, Inc.), ATG5 (1:1,000; catalog no. NB110-53818, lot no. RRID:AB_828587, Novus Biologicals), p62 (1:1,000; catalog no. 50–507-55, lot no. RRID: AB_2571590; Thermo Fisher Scientific), LC3 (1:2,000; catalog no. NB100-2220, lot no. RRID:AB_10003146; Novus Biologicals), and β-actin (1:5,000; catalog no. A1978, lot no. RRID:AB_476692; Sigma-Aldrich).

Techniques: Western Blot, Injection, Saline, Expressing, Staining, Plasmid Preparation, In Vitro, Control

Morphine-mediated autophagy in hippocampal neurons: Role of oxidative and ER stress. Representative Western blot (A) and quantification of autophagy mediators (Beclin1, ATG5, p62, and LC3-II; B) in the cell lysates of neurons pretreated with PBN or apocynin for 1 h followed by 24-h morphine treatment. (C) H 2 DCFDA assay of neurons pretreated with 3-MA (50 µM) for 30 min followed by morphine exposure. Representative Western blot (D) and quantification of Beclin1, ATG5, p62, and LC3-II (E) in the cell lysates of neurons pretreated with 4-PBA or salubrinal (100 µM) for 1 h followed by 24-h morphine exposure. Representative Western blot (F) and quantification of BIP, pPERK, IRE1α, and ATF6 (G) in the cell lysates of neurons pretreated with wortmannin or 3-MA for 1 h followed by 24-h morphine exposure. Quantification of Western blot results were all normalized to β-actin, except that pPERK was normalized to PERK. Each set of our results was quantified upon four independent experiments. All data are presented as mean ± SD. *, P < 0.05; **, P < 0.01 versus control/saline group; # , P < 0.05; ## , P < 0.01 versus morphine group using one-way ANOVA with post hoc test.

Journal: The Journal of Cell Biology

Article Title: Regulation of morphine-induced synaptic alterations: Role of oxidative stress, ER stress, and autophagy

doi: 10.1083/jcb.201605065

Figure Lengend Snippet: Morphine-mediated autophagy in hippocampal neurons: Role of oxidative and ER stress. Representative Western blot (A) and quantification of autophagy mediators (Beclin1, ATG5, p62, and LC3-II; B) in the cell lysates of neurons pretreated with PBN or apocynin for 1 h followed by 24-h morphine treatment. (C) H 2 DCFDA assay of neurons pretreated with 3-MA (50 µM) for 30 min followed by morphine exposure. Representative Western blot (D) and quantification of Beclin1, ATG5, p62, and LC3-II (E) in the cell lysates of neurons pretreated with 4-PBA or salubrinal (100 µM) for 1 h followed by 24-h morphine exposure. Representative Western blot (F) and quantification of BIP, pPERK, IRE1α, and ATF6 (G) in the cell lysates of neurons pretreated with wortmannin or 3-MA for 1 h followed by 24-h morphine exposure. Quantification of Western blot results were all normalized to β-actin, except that pPERK was normalized to PERK. Each set of our results was quantified upon four independent experiments. All data are presented as mean ± SD. *, P < 0.05; **, P < 0.01 versus control/saline group; # , P < 0.05; ## , P < 0.01 versus morphine group using one-way ANOVA with post hoc test.

Article Snippet: The Western blots were then probed with respective antibodies recognizing the vGlut1 (1:5,000; catalog no. AB5905, lot no. RRID:AB_2301751; EMD Millipore), PSD95 (1:1,000; catalog no. ab18258; lot no. RRID:AB_444362; Abcam), GAD65 (1:1,000; catalog no. NBP1-33284, lot no. RRID:AB_10004060; Novus Biologicals), gephyrin (1:250; catalog no. 610584, lot no. RRID:AB_397929; BD), BIP (1:1,000; catalog no. 610978, lot no. RRID:AB_398291; BD), pPERK (1:250; catalog no. sc-32577, lot no. RRID:AB_2293243; Santa Cruz Biotechnology, Inc.), PERK (1:250; catalog no. sc-13073, lot no. RRID:AB_2230863; Santa Cruz Biotechnology, Inc.), IRE1α (1:500; catalog no. sc-20790, lot no. RRID:AB_2098712; Santa Cruz Biotechnology, Inc.), ATF6 (1:1,000; catalog no. ab37149, lot no. RRID:AB_725571; Abcam), Beclin1 (1:1,000; catalog no. sc-11427, lot no. RRID:AB_2064465; Santa Cruz Biotechnology, Inc.), ATG5 (1:1,000; catalog no. NB110-53818, lot no. RRID:AB_828587, Novus Biologicals), p62 (1:1,000; catalog no. 50–507-55, lot no. RRID: AB_2571590; Thermo Fisher Scientific), LC3 (1:2,000; catalog no. NB100-2220, lot no. RRID:AB_10003146; Novus Biologicals), and β-actin (1:5,000; catalog no. A1978, lot no. RRID:AB_476692; Sigma-Aldrich).

Techniques: Western Blot, Control, Saline

Protective role of PDGF-BB in morphine-mediated synaptic alterations. Representative confocal images of GFP-expressing primary rat hippocampal neurons exposed to morphine followed by treatment with PDGF-BB (20 ng/ml) and stained with vGlut1 and GAD65 (A) and quantifications of spine density and excitatory and inhibitory synapses (B). Bar, 5 µm. Representative traces of whole-cell voltage-clamp recording showing mEPSC (C), mIPSC (E), mean mEPSC frequencies (D), and mean frequencies of mIPSCs (Hz; F) in primary rat neurons (DIV 19–21) treated with combinations of saline, morphine, and PDGF-BB as indicated. (G) ROS generation in neurons exposed to morphine and treated with PDGF-BB. Representative Western blot (H) and quantification of BIP, pPERK, IRE1α, and ATF6 (I) in the cell lysates of neurons exposed to morphine followed by treatment with PDGF-BB (20 ng/ml) for an additional 24 h. Representative Western blot (J) and quantification of Beclin1, ATG5, p62, and LC3-II (K) in the cell lysates of neurons exposed to morphine for 24 h followed by PDGF-BB (20 ng/ml) for additional 24 h. Quantification of Western blot results were all normalized to β-actin except that pPERK was normalized to PERK. Each set of our results was quantified upon four independent experiments. All data are presented as mean ± SD. *, P < 0.05; **, P < 0.01 versus control/saline group; # , P < 0.05; ## , P < 0.01 versus morphine group using one-way ANOVA with post hoc test.

Journal: The Journal of Cell Biology

Article Title: Regulation of morphine-induced synaptic alterations: Role of oxidative stress, ER stress, and autophagy

doi: 10.1083/jcb.201605065

Figure Lengend Snippet: Protective role of PDGF-BB in morphine-mediated synaptic alterations. Representative confocal images of GFP-expressing primary rat hippocampal neurons exposed to morphine followed by treatment with PDGF-BB (20 ng/ml) and stained with vGlut1 and GAD65 (A) and quantifications of spine density and excitatory and inhibitory synapses (B). Bar, 5 µm. Representative traces of whole-cell voltage-clamp recording showing mEPSC (C), mIPSC (E), mean mEPSC frequencies (D), and mean frequencies of mIPSCs (Hz; F) in primary rat neurons (DIV 19–21) treated with combinations of saline, morphine, and PDGF-BB as indicated. (G) ROS generation in neurons exposed to morphine and treated with PDGF-BB. Representative Western blot (H) and quantification of BIP, pPERK, IRE1α, and ATF6 (I) in the cell lysates of neurons exposed to morphine followed by treatment with PDGF-BB (20 ng/ml) for an additional 24 h. Representative Western blot (J) and quantification of Beclin1, ATG5, p62, and LC3-II (K) in the cell lysates of neurons exposed to morphine for 24 h followed by PDGF-BB (20 ng/ml) for additional 24 h. Quantification of Western blot results were all normalized to β-actin except that pPERK was normalized to PERK. Each set of our results was quantified upon four independent experiments. All data are presented as mean ± SD. *, P < 0.05; **, P < 0.01 versus control/saline group; # , P < 0.05; ## , P < 0.01 versus morphine group using one-way ANOVA with post hoc test.

Article Snippet: The Western blots were then probed with respective antibodies recognizing the vGlut1 (1:5,000; catalog no. AB5905, lot no. RRID:AB_2301751; EMD Millipore), PSD95 (1:1,000; catalog no. ab18258; lot no. RRID:AB_444362; Abcam), GAD65 (1:1,000; catalog no. NBP1-33284, lot no. RRID:AB_10004060; Novus Biologicals), gephyrin (1:250; catalog no. 610584, lot no. RRID:AB_397929; BD), BIP (1:1,000; catalog no. 610978, lot no. RRID:AB_398291; BD), pPERK (1:250; catalog no. sc-32577, lot no. RRID:AB_2293243; Santa Cruz Biotechnology, Inc.), PERK (1:250; catalog no. sc-13073, lot no. RRID:AB_2230863; Santa Cruz Biotechnology, Inc.), IRE1α (1:500; catalog no. sc-20790, lot no. RRID:AB_2098712; Santa Cruz Biotechnology, Inc.), ATF6 (1:1,000; catalog no. ab37149, lot no. RRID:AB_725571; Abcam), Beclin1 (1:1,000; catalog no. sc-11427, lot no. RRID:AB_2064465; Santa Cruz Biotechnology, Inc.), ATG5 (1:1,000; catalog no. NB110-53818, lot no. RRID:AB_828587, Novus Biologicals), p62 (1:1,000; catalog no. 50–507-55, lot no. RRID: AB_2571590; Thermo Fisher Scientific), LC3 (1:2,000; catalog no. NB100-2220, lot no. RRID:AB_10003146; Novus Biologicals), and β-actin (1:5,000; catalog no. A1978, lot no. RRID:AB_476692; Sigma-Aldrich).

Techniques: Expressing, Staining, Saline, Western Blot, Control

RT-qPCR validation of hub gene expression following autophagy modulation and photodynamic therapy (PDT). RT-qPCR analysis showing relative mRNA expression levels of autophagy-related hub genes (AKT1, BCL2, BECN1, ATG5) in NPC cell lines (C666-1 and HONE1) under different conditions: control, PDT alone, autophagy activation (rapamycin + PDT), and autophagy inhibition (chloroquine + PDT). Autophagy activation amplified the transcriptional induction of BECN1 and ATG5, whereas inhibition suppressed their expression, indicating that autophagy promotes survival signaling during PDT stress. P -value < 0.05

Journal: Journal of Molecular Histology

Article Title: Autophagy hub genes mediate photodynamic therapy tolerance in nasopharyngeal carcinoma through cytoprotective autophagy and survival signaling

doi: 10.1007/s10735-026-10746-x

Figure Lengend Snippet: RT-qPCR validation of hub gene expression following autophagy modulation and photodynamic therapy (PDT). RT-qPCR analysis showing relative mRNA expression levels of autophagy-related hub genes (AKT1, BCL2, BECN1, ATG5) in NPC cell lines (C666-1 and HONE1) under different conditions: control, PDT alone, autophagy activation (rapamycin + PDT), and autophagy inhibition (chloroquine + PDT). Autophagy activation amplified the transcriptional induction of BECN1 and ATG5, whereas inhibition suppressed their expression, indicating that autophagy promotes survival signaling during PDT stress. P -value < 0.05

Article Snippet: Membranes were blocked in 5% non-fat milk in TBST and incubated overnight at 4 °C with primary antibodies against AKT1 (CST #2938, 1:1000), BECN1/Beclin-1 (CST #3738, 1:1000), BCL2 (CST #2876, 1:1000), ATG5 (CST #2630, 1:1000), LC3B (CST #3868, 1:1000), p62/SQSTM1 (CST #5114, 1:1000), and the loading control GAPDH (CST #2118, 1:5000).

Techniques: Quantitative RT-PCR, Biomarker Discovery, Gene Expression, Expressing, Control, Activation Assay, Inhibition, Amplification

Western blot analysis of autophagy hub proteins following PDT and autophagy modulation. Protein expression of BCL2, AKT1, BECN1, and ATG5 in A C666-1 and B HONE1 cells following PDT, autophagy activation (rapamycin + PDT), or inhibition (chloroquine + PDT). Autophagy activation enhanced expression of both autophagic and pro-survival proteins, while inhibition blunted induction

Journal: Journal of Molecular Histology

Article Title: Autophagy hub genes mediate photodynamic therapy tolerance in nasopharyngeal carcinoma through cytoprotective autophagy and survival signaling

doi: 10.1007/s10735-026-10746-x

Figure Lengend Snippet: Western blot analysis of autophagy hub proteins following PDT and autophagy modulation. Protein expression of BCL2, AKT1, BECN1, and ATG5 in A C666-1 and B HONE1 cells following PDT, autophagy activation (rapamycin + PDT), or inhibition (chloroquine + PDT). Autophagy activation enhanced expression of both autophagic and pro-survival proteins, while inhibition blunted induction

Article Snippet: Membranes were blocked in 5% non-fat milk in TBST and incubated overnight at 4 °C with primary antibodies against AKT1 (CST #2938, 1:1000), BECN1/Beclin-1 (CST #3738, 1:1000), BCL2 (CST #2876, 1:1000), ATG5 (CST #2630, 1:1000), LC3B (CST #3868, 1:1000), p62/SQSTM1 (CST #5114, 1:1000), and the loading control GAPDH (CST #2118, 1:5000).

Techniques: Western Blot, Expressing, Activation Assay, Inhibition

Genetic depletion of ATG5 and BECN1 enhances photodynamic therapy sensitivity in nasopharyngeal carcinoma cells. A - B siRNA-mediated knockdown of ATG5 or BECN in C666-1 cells significantly reduced target mRNA expression as confirmed by RT-qPCR. Functional analyses demonstrated that PDT significantly decreased cell viability and clonogenic survival in control cells, and that genetic depletion of ATG5 or BECN1 further enhanced PDT-induced cytotoxicity. C - D siRNA-mediated knockdown of ATG5 or BECN in HONE1 cells significantly reduced target mRNA expression as confirmed by RT-qPCR. Functional analyses demonstrated that PDT significantly decreased cell viability and clonogenic survival in control cells, and that genetic depletion of ATG5 or BECN1 further enhanced PDT-induced cytotoxicity. P -value* < 0.05, P **-value < 0.01, P ***-value < 0.001

Journal: Journal of Molecular Histology

Article Title: Autophagy hub genes mediate photodynamic therapy tolerance in nasopharyngeal carcinoma through cytoprotective autophagy and survival signaling

doi: 10.1007/s10735-026-10746-x

Figure Lengend Snippet: Genetic depletion of ATG5 and BECN1 enhances photodynamic therapy sensitivity in nasopharyngeal carcinoma cells. A - B siRNA-mediated knockdown of ATG5 or BECN in C666-1 cells significantly reduced target mRNA expression as confirmed by RT-qPCR. Functional analyses demonstrated that PDT significantly decreased cell viability and clonogenic survival in control cells, and that genetic depletion of ATG5 or BECN1 further enhanced PDT-induced cytotoxicity. C - D siRNA-mediated knockdown of ATG5 or BECN in HONE1 cells significantly reduced target mRNA expression as confirmed by RT-qPCR. Functional analyses demonstrated that PDT significantly decreased cell viability and clonogenic survival in control cells, and that genetic depletion of ATG5 or BECN1 further enhanced PDT-induced cytotoxicity. P -value* < 0.05, P **-value < 0.01, P ***-value < 0.001

Article Snippet: Membranes were blocked in 5% non-fat milk in TBST and incubated overnight at 4 °C with primary antibodies against AKT1 (CST #2938, 1:1000), BECN1/Beclin-1 (CST #3738, 1:1000), BCL2 (CST #2876, 1:1000), ATG5 (CST #2630, 1:1000), LC3B (CST #3868, 1:1000), p62/SQSTM1 (CST #5114, 1:1000), and the loading control GAPDH (CST #2118, 1:5000).

Techniques: Knockdown, Expressing, Quantitative RT-PCR, Functional Assay, Control

Genetic alterations in autophagy hub genes in head and neck squamous cell carcinoma (HNSC). A Frequency of genomic alterations in AKT1, BECN1, BCL2, and ATG5 across HNSC samples from cBioPortal. B Mutation mapping within functional domains of each gene

Journal: Journal of Molecular Histology

Article Title: Autophagy hub genes mediate photodynamic therapy tolerance in nasopharyngeal carcinoma through cytoprotective autophagy and survival signaling

doi: 10.1007/s10735-026-10746-x

Figure Lengend Snippet: Genetic alterations in autophagy hub genes in head and neck squamous cell carcinoma (HNSC). A Frequency of genomic alterations in AKT1, BECN1, BCL2, and ATG5 across HNSC samples from cBioPortal. B Mutation mapping within functional domains of each gene

Article Snippet: Membranes were blocked in 5% non-fat milk in TBST and incubated overnight at 4 °C with primary antibodies against AKT1 (CST #2938, 1:1000), BECN1/Beclin-1 (CST #3738, 1:1000), BCL2 (CST #2876, 1:1000), ATG5 (CST #2630, 1:1000), LC3B (CST #3868, 1:1000), p62/SQSTM1 (CST #5114, 1:1000), and the loading control GAPDH (CST #2118, 1:5000).

Techniques: Mutagenesis, Functional Assay

Prognostic, epigenetic, immune, and pharmacologic associations of autophagy hub genes in HNSC. A Kaplan–Meier overall survival analysis showing high expression of BCL2, AKT1, BECN1, and ATG5 associated with poorer prognosis. B Promoter methylation analysis from GSCA showing hypomethylation of hub genes in tumor versus control samples. C Inverse correlation between promoter methylation and gene expression across HNSC samples. D Immune infiltration analysis revealing associations of hub gene expression with macrophages, NK cells, and T-cell subsets. E Drug sensitivity correlations (GDSC) showing gene expression–dependent responses to anticancer agents, with BCL2 expression linked to increased drug sensitivity and AKT1 linked to resistance. P -value < 0.05

Journal: Journal of Molecular Histology

Article Title: Autophagy hub genes mediate photodynamic therapy tolerance in nasopharyngeal carcinoma through cytoprotective autophagy and survival signaling

doi: 10.1007/s10735-026-10746-x

Figure Lengend Snippet: Prognostic, epigenetic, immune, and pharmacologic associations of autophagy hub genes in HNSC. A Kaplan–Meier overall survival analysis showing high expression of BCL2, AKT1, BECN1, and ATG5 associated with poorer prognosis. B Promoter methylation analysis from GSCA showing hypomethylation of hub genes in tumor versus control samples. C Inverse correlation between promoter methylation and gene expression across HNSC samples. D Immune infiltration analysis revealing associations of hub gene expression with macrophages, NK cells, and T-cell subsets. E Drug sensitivity correlations (GDSC) showing gene expression–dependent responses to anticancer agents, with BCL2 expression linked to increased drug sensitivity and AKT1 linked to resistance. P -value < 0.05

Article Snippet: Membranes were blocked in 5% non-fat milk in TBST and incubated overnight at 4 °C with primary antibodies against AKT1 (CST #2938, 1:1000), BECN1/Beclin-1 (CST #3738, 1:1000), BCL2 (CST #2876, 1:1000), ATG5 (CST #2630, 1:1000), LC3B (CST #3868, 1:1000), p62/SQSTM1 (CST #5114, 1:1000), and the loading control GAPDH (CST #2118, 1:5000).

Techniques: Expressing, Methylation, Control, Gene Expression

Proposed mechanistic model linking autophagy hubs to PDT tolerance in nasopharyngeal carcinoma. Schematic diagram summarizing the proposed mechanism. Photodynamic therapy induces ROS generation and autophagic stress. BECN1 and ATG5 promote autophagosome formation, while BCL2 and AKT1 mediate survival signaling through the mTOR and BCL2–BECN1 axes. This coordinated response leads to enhanced cytoprotective autophagy, organelle clearance, and apoptosis suppression, contributing to PDT resistance. Targeting late-stage autophagy or disrupting the BCL2–BECN1 and AKT/mTOR pathways may restore PDT sensitivity

Journal: Journal of Molecular Histology

Article Title: Autophagy hub genes mediate photodynamic therapy tolerance in nasopharyngeal carcinoma through cytoprotective autophagy and survival signaling

doi: 10.1007/s10735-026-10746-x

Figure Lengend Snippet: Proposed mechanistic model linking autophagy hubs to PDT tolerance in nasopharyngeal carcinoma. Schematic diagram summarizing the proposed mechanism. Photodynamic therapy induces ROS generation and autophagic stress. BECN1 and ATG5 promote autophagosome formation, while BCL2 and AKT1 mediate survival signaling through the mTOR and BCL2–BECN1 axes. This coordinated response leads to enhanced cytoprotective autophagy, organelle clearance, and apoptosis suppression, contributing to PDT resistance. Targeting late-stage autophagy or disrupting the BCL2–BECN1 and AKT/mTOR pathways may restore PDT sensitivity

Article Snippet: Membranes were blocked in 5% non-fat milk in TBST and incubated overnight at 4 °C with primary antibodies against AKT1 (CST #2938, 1:1000), BECN1/Beclin-1 (CST #3738, 1:1000), BCL2 (CST #2876, 1:1000), ATG5 (CST #2630, 1:1000), LC3B (CST #3868, 1:1000), p62/SQSTM1 (CST #5114, 1:1000), and the loading control GAPDH (CST #2118, 1:5000).

Techniques:

Figure 1 M. hyopneumoniae infection increases the formation of autophagosome-like vesicles and the expression of autophagy-related proteins in porcine alveolar macrophages. A Autophagosome-like vesicles (arrows) were observed in M. hyopneumoniae-negative (a) and M. hyopneumoniae-positive (b) PAMs by TEM. Ten M. hyopneumoniae-negative and 10 M. hyopneumoniae-positive PAMs were assessed. B Autophagosome-like vesicles (arrows) were observed in mock-infected (a) or AH-infected (b) 3D4/21 cells by TEM. Ten uninfected and 10 AH-infected 3D4/21 cells were assessed. C Results of Western blotting showing the expression of autophagy-related proteins (LC3-II, Atg5, Atg12-Atg5, and Beclin 1) and Mhp366 in 30 M. hyopneumoniae-positive and 10 M. hyopneumoniae-negative PAMs collected from pigs. D Results of Western blotting showing the expression of autophagy-related proteins (LC3-II, Atg5, Atg12-Atg5, and Beclin 1) and P97 protein in 3D4/21 cells after mock infection or AH infection. Mean values from 3 independent experiments are presented. Between-group differences were assessed using a t test; *p ≤ 0.05, **p ≤ 0.01.

Journal: Veterinary research

Article Title: Incomplete autophagy promotes the proliferation of Mycoplasma hyopneumoniae through the JNK and Akt pathways in porcine alveolar macrophages.

doi: 10.1186/s13567-022-01074-5

Figure Lengend Snippet: Figure 1 M. hyopneumoniae infection increases the formation of autophagosome-like vesicles and the expression of autophagy-related proteins in porcine alveolar macrophages. A Autophagosome-like vesicles (arrows) were observed in M. hyopneumoniae-negative (a) and M. hyopneumoniae-positive (b) PAMs by TEM. Ten M. hyopneumoniae-negative and 10 M. hyopneumoniae-positive PAMs were assessed. B Autophagosome-like vesicles (arrows) were observed in mock-infected (a) or AH-infected (b) 3D4/21 cells by TEM. Ten uninfected and 10 AH-infected 3D4/21 cells were assessed. C Results of Western blotting showing the expression of autophagy-related proteins (LC3-II, Atg5, Atg12-Atg5, and Beclin 1) and Mhp366 in 30 M. hyopneumoniae-positive and 10 M. hyopneumoniae-negative PAMs collected from pigs. D Results of Western blotting showing the expression of autophagy-related proteins (LC3-II, Atg5, Atg12-Atg5, and Beclin 1) and P97 protein in 3D4/21 cells after mock infection or AH infection. Mean values from 3 independent experiments are presented. Between-group differences were assessed using a t test; *p ≤ 0.05, **p ≤ 0.01.

Article Snippet: Polyclonal antibodies against ATG5 (NBP2-24389), ATG5 (NB11053818), Beclin 1 (NB110-87318), and p62 (NBP1-48320) were purchased from Novus Biologicals (Shanghai, China).

Techniques: Infection, Expressing, Western Blot