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mitophagy antibody sampler kit  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc mitophagy antibody sampler kit
    Changes in mitochondrial function following ECHDC3 knockdown. (A) TMRE staining results based on ECHDC3 -knockdown cells. siNC cells emitted bright red-orange fluorescence. Cells treated with a mitochondrial membrane-potential disrupter, CCCP, showed very weak or complete absence of red-orange fluorescence. The average fluorescence intensity of the cells was calculated and quantitatively analyzed. (B–C) mtDNA copy number ( MT–CO1 and MT–CO2 ) was quantified via quantitative RT-PCR; (D) Quantitation of mitochondrial SOD activity, wherein SOD activity decreased in ECHDC3 -knockdown cells. (E) <t>Mitophagy</t> biomarkers were detected via western blotting. β-Actin was used as a control. (F–I) Quantitation of the mitophagy pathway protein. Values were presented as mean ± standard error. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. CCCP: Carbonyl cyanide m-chlorophenyl hydrazone; ECHDC3 : Enoyl-CoA hydratase domain-containing protein 3; mtDNA: Mitochondrial DNA; RT-PCR: Real-time polymerase chain reaction; SOD: Superoxide dismutase; TMRE: Tetramethyl rhodamine ethyl ester.
    Mitophagy Antibody Sampler Kit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mitophagy+antibody+sampler+kit/pmc13000501-63-13-19
    Average 86 stars, based on 1 article reviews
    mitophagy antibody sampler kit - by Bioz Stars, 2026-09
    86/100 stars

    Images

    1) Product Images from "Metabolic pathways and chemotherapy resistance in acute myeloid leukemia (AML): Insights into Enoyl-CoA hydratase domain-containing protein 3 ( ECHDC3 ) as a potential therapeutic target"

    Article Title: Metabolic pathways and chemotherapy resistance in acute myeloid leukemia (AML): Insights into Enoyl-CoA hydratase domain-containing protein 3 ( ECHDC3 ) as a potential therapeutic target

    Journal: Cancer Pathogenesis and Therapy

    doi: 10.1016/j.cpt.2025.08.002

    Changes in mitochondrial function following ECHDC3 knockdown. (A) TMRE staining results based on ECHDC3 -knockdown cells. siNC cells emitted bright red-orange fluorescence. Cells treated with a mitochondrial membrane-potential disrupter, CCCP, showed very weak or complete absence of red-orange fluorescence. The average fluorescence intensity of the cells was calculated and quantitatively analyzed. (B–C) mtDNA copy number ( MT–CO1 and MT–CO2 ) was quantified via quantitative RT-PCR; (D) Quantitation of mitochondrial SOD activity, wherein SOD activity decreased in ECHDC3 -knockdown cells. (E) Mitophagy biomarkers were detected via western blotting. β-Actin was used as a control. (F–I) Quantitation of the mitophagy pathway protein. Values were presented as mean ± standard error. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. CCCP: Carbonyl cyanide m-chlorophenyl hydrazone; ECHDC3 : Enoyl-CoA hydratase domain-containing protein 3; mtDNA: Mitochondrial DNA; RT-PCR: Real-time polymerase chain reaction; SOD: Superoxide dismutase; TMRE: Tetramethyl rhodamine ethyl ester.
    Figure Legend Snippet: Changes in mitochondrial function following ECHDC3 knockdown. (A) TMRE staining results based on ECHDC3 -knockdown cells. siNC cells emitted bright red-orange fluorescence. Cells treated with a mitochondrial membrane-potential disrupter, CCCP, showed very weak or complete absence of red-orange fluorescence. The average fluorescence intensity of the cells was calculated and quantitatively analyzed. (B–C) mtDNA copy number ( MT–CO1 and MT–CO2 ) was quantified via quantitative RT-PCR; (D) Quantitation of mitochondrial SOD activity, wherein SOD activity decreased in ECHDC3 -knockdown cells. (E) Mitophagy biomarkers were detected via western blotting. β-Actin was used as a control. (F–I) Quantitation of the mitophagy pathway protein. Values were presented as mean ± standard error. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. CCCP: Carbonyl cyanide m-chlorophenyl hydrazone; ECHDC3 : Enoyl-CoA hydratase domain-containing protein 3; mtDNA: Mitochondrial DNA; RT-PCR: Real-time polymerase chain reaction; SOD: Superoxide dismutase; TMRE: Tetramethyl rhodamine ethyl ester.

    Techniques Used: Knockdown, Staining, Fluorescence, Membrane, Quantitative RT-PCR, Quantitation Assay, Activity Assay, Western Blot, Control, Reverse Transcription Polymerase Chain Reaction, Real-time Polymerase Chain Reaction

    Related Articles

    Blocking Assay:

    Article Title: Human papillomavirus E7 inhibits immune responses in keratinocytes by activating HTRA1‑mediated mitophagy.
    Article Snippet: After protein extraction, the protein samples (10 μg/lane) were separated by SdS‐PAGE on 12% gels and were subse‐ quently transferred onto polyvinylidene fluoride membranes (0.2 μm; cat. no. 1620177; Bio‐Rad Laboratories, Inc.) using a wet transblotting apparatus (Bio‐Rad Laboratories, Inc.). .. Upon blocking with 10% nonfat milk (difco; Bd Biosciences) for 1 h at room temperature, the membranes were incubated over‐ night with the following primary antibodies diluted to 1:1,000 in primary antibody diluent (cat. no. Fd0040; Hangzhou Fude Biological Technology co., Ltd.): Mitophagy Antibody Sampler kit (cat. no. 43110; cell Signaling Technology, Inc.), polyclonal rabbit anti‐HTRA1 (cat. no. SAB1300009; Sigma‐Aldrich; Merck KGaA), polyclonal rabbit anti‐Lc3B (cat. no. L8918; Sigma‐Aldrich; Merck KGaA), monoclonal mouse anti‐GAPdH (cat. no. G8795; Sigma‐Aldrich; Merck KGaA), monoclonal rabbit anti‐p62 (cat. no. ab109012; Abcam), anti‐Flag (cat. no. M1403‐2; HUABIO), polyclonal rabbit anti‐HPV11/16 E7 (prepared in our laboratory) (62‐65) and monoclonal rabbit anti‐pRB (cat. no. ab181616; Abcam). .. After washing the membranes three times with PBS (10 min each), they were incubated for 2 h at room temperature with horseradish peroxidase (HRP)‐conjugated goat anti‐rabbit IgG (H+L; cat. no. A0208; Beyotime Institute of Biotechnology) or HRP‐conjugated goat anti‐mouse IgG (H+L; cat. no. A0216; Beyotime Institute of Biotechnology) secondary antibodies diluted to 1:500 in 5% skimmed milk.

    Article Title: Human papillomavirus E7 inhibits immune responses in keratinocytes by activating HTRA1-mediated mitophagy
    Article Snippet: After protein extraction, the protein samples (10 μ g/lane) were separated by SDS-PAGE on 12% gels and were subsequently transferred onto polyvinylidene fluoride membranes (0.2 μ m; cat. no. 1620177; Bio-Rad Laboratories, Inc.) using a wet transblotting apparatus (Bio-Rad Laboratories, Inc.). .. Upon blocking with 10% nonfat milk (Difco; BD Biosciences) for 1 h at room temperature, the membranes were incubated overnight with the following primary antibodies diluted to 1:1,000 in primary antibody diluent (cat. no. FD0040; Hangzhou Fude Biological Technology Co., Ltd.): Mitophagy Antibody Sampler kit (cat. no. 43110; Cell Signaling Technology, Inc.), polyclonal rabbit anti-HTRA1 (cat. no. SAB1300009; Sigma-Aldrich; Merck KGaA), polyclonal rabbit anti-LC3B (cat. no. L8918; Sigma-Aldrich; Merck KGaA), monoclonal mouse anti-GAPDH (cat. no. G8795; Sigma-Aldrich; Merck KGaA), monoclonal rabbit anti-p62 (cat. no. ab109012; Abcam), anti-Flag (cat. no. M1403-2; HUABIO), polyclonal rabbit anti-HPV11/16 E7 (prepared in our laboratory) ( - ) and monoclonal rabbit anti-pRB (cat. no. ab181616; Abcam). .. After washing the membranes three times with PBS (10 min each), they were incubated for 2 h at room temperature with horseradish peroxidase (HRP)-conjugated goat anti-rabbit IgG (H+L; cat. no. A0208; Beyotime Institute of Biotechnology) or HRP-conjugated goat anti-mouse IgG (H+L; cat. no. A0216; Beyotime Institute of Biotechnology) secondary antibodies diluted to 1:500 in 5% skimmed milk.

    Incubation:

    Article Title: Human papillomavirus E7 inhibits immune responses in keratinocytes by activating HTRA1‑mediated mitophagy.
    Article Snippet: After protein extraction, the protein samples (10 μg/lane) were separated by SdS‐PAGE on 12% gels and were subse‐ quently transferred onto polyvinylidene fluoride membranes (0.2 μm; cat. no. 1620177; Bio‐Rad Laboratories, Inc.) using a wet transblotting apparatus (Bio‐Rad Laboratories, Inc.). .. Upon blocking with 10% nonfat milk (difco; Bd Biosciences) for 1 h at room temperature, the membranes were incubated over‐ night with the following primary antibodies diluted to 1:1,000 in primary antibody diluent (cat. no. Fd0040; Hangzhou Fude Biological Technology co., Ltd.): Mitophagy Antibody Sampler kit (cat. no. 43110; cell Signaling Technology, Inc.), polyclonal rabbit anti‐HTRA1 (cat. no. SAB1300009; Sigma‐Aldrich; Merck KGaA), polyclonal rabbit anti‐Lc3B (cat. no. L8918; Sigma‐Aldrich; Merck KGaA), monoclonal mouse anti‐GAPdH (cat. no. G8795; Sigma‐Aldrich; Merck KGaA), monoclonal rabbit anti‐p62 (cat. no. ab109012; Abcam), anti‐Flag (cat. no. M1403‐2; HUABIO), polyclonal rabbit anti‐HPV11/16 E7 (prepared in our laboratory) (62‐65) and monoclonal rabbit anti‐pRB (cat. no. ab181616; Abcam). .. After washing the membranes three times with PBS (10 min each), they were incubated for 2 h at room temperature with horseradish peroxidase (HRP)‐conjugated goat anti‐rabbit IgG (H+L; cat. no. A0208; Beyotime Institute of Biotechnology) or HRP‐conjugated goat anti‐mouse IgG (H+L; cat. no. A0216; Beyotime Institute of Biotechnology) secondary antibodies diluted to 1:500 in 5% skimmed milk.

    Article Title: Human papillomavirus E7 inhibits immune responses in keratinocytes by activating HTRA1-mediated mitophagy
    Article Snippet: After protein extraction, the protein samples (10 μ g/lane) were separated by SDS-PAGE on 12% gels and were subsequently transferred onto polyvinylidene fluoride membranes (0.2 μ m; cat. no. 1620177; Bio-Rad Laboratories, Inc.) using a wet transblotting apparatus (Bio-Rad Laboratories, Inc.). .. Upon blocking with 10% nonfat milk (Difco; BD Biosciences) for 1 h at room temperature, the membranes were incubated overnight with the following primary antibodies diluted to 1:1,000 in primary antibody diluent (cat. no. FD0040; Hangzhou Fude Biological Technology Co., Ltd.): Mitophagy Antibody Sampler kit (cat. no. 43110; Cell Signaling Technology, Inc.), polyclonal rabbit anti-HTRA1 (cat. no. SAB1300009; Sigma-Aldrich; Merck KGaA), polyclonal rabbit anti-LC3B (cat. no. L8918; Sigma-Aldrich; Merck KGaA), monoclonal mouse anti-GAPDH (cat. no. G8795; Sigma-Aldrich; Merck KGaA), monoclonal rabbit anti-p62 (cat. no. ab109012; Abcam), anti-Flag (cat. no. M1403-2; HUABIO), polyclonal rabbit anti-HPV11/16 E7 (prepared in our laboratory) ( - ) and monoclonal rabbit anti-pRB (cat. no. ab181616; Abcam). .. After washing the membranes three times with PBS (10 min each), they were incubated for 2 h at room temperature with horseradish peroxidase (HRP)-conjugated goat anti-rabbit IgG (H+L; cat. no. A0208; Beyotime Institute of Biotechnology) or HRP-conjugated goat anti-mouse IgG (H+L; cat. no. A0216; Beyotime Institute of Biotechnology) secondary antibodies diluted to 1:500 in 5% skimmed milk.

    Western Blot:

    Article Title: RMRP-Induced Chemo-Resistance in Relapsed and Refractory Acute Myeloid Leukemia via Mitochondrial Dysfunction.
    Article Snippet: .. Western blotting was performed to detect mitochondrial autophagy proteins, using the Mitophagy Antibody Sampler Kit (Cat# 43110, Cell Signaling Technology [CST]) and an anti-β-actin (Cat# 8H10D10, CST) mouse mAb (Cat# 3700, CST). .. The blots were developed using a Bio-Rad Imaging System.

    Article Title: Metabolic pathways and chemotherapy resistance in acute myeloid leukemia (AML): Insights into Enoyl-CoA hydratase domain-containing protein 3 ( ECHDC3 ) as a potential therapeutic target
    Article Snippet: Library quality was assessed using the Agilent Bioanalyzer 2100 system. .. Western blotting was performed to determine the expression of mitochondrial proteins, using the Mitophagy Antibody Sampler Kit (Cat# 43110, Cell Signaling Technology [CST], MA, USA) and an anti-β-actin mouse monoclonal antibody (Cat# 3700, CST, MA, USA). .. Blots were developed using a Bio-Rad Imaging System.

    other:

    Article Title: β-amyloid protein induces mitophagy-dependent ferroptosis through the CD36/PINK/PARKIN pathway leading to blood–brain barrier destruction in Alzheimer’s disease
    Article Snippet: The following antibodies were used in this study: β-amyloid (20.1) (Santa Cruz Biotechnology); PDGFRβ (Abcam and CST); NG2 (Abcam); LRP1 (Abcam); CD36 (ABclonal); CD31 (CST); GLUT1 (Abcam); CD36 (BD); β-actin (ABclonal); HSP60 (Santa Cruz Biotechnology); Tim23 (ABclonal); LC3B (Sigma–Aldrich); cleaved-caspase 3 (CST); caspase 3 (ABclonal); BAX (ABclonal); BCL2 (ABclonal); GPx4 (Proteintech); xCT (Proteintech); NOX1 (Proteintech); GAPDH (Proteintech); ferritin (Beyotime); and a Mitophagy Antibody Sampler Kit (CST).

    Expressing:

    Article Title: Metabolic pathways and chemotherapy resistance in acute myeloid leukemia (AML): Insights into Enoyl-CoA hydratase domain-containing protein 3 ( ECHDC3 ) as a potential therapeutic target
    Article Snippet: Library quality was assessed using the Agilent Bioanalyzer 2100 system. .. Western blotting was performed to determine the expression of mitochondrial proteins, using the Mitophagy Antibody Sampler Kit (Cat# 43110, Cell Signaling Technology [CST], MA, USA) and an anti-β-actin mouse monoclonal antibody (Cat# 3700, CST, MA, USA). .. Blots were developed using a Bio-Rad Imaging System.



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    Changes in mitochondrial function following ECHDC3 knockdown. (A) TMRE staining results based on ECHDC3 -knockdown cells. siNC cells emitted bright red-orange fluorescence. Cells treated with a mitochondrial membrane-potential disrupter, CCCP, showed very weak or complete absence of red-orange fluorescence. The average fluorescence intensity of the cells was calculated and quantitatively analyzed. (B–C) mtDNA copy number ( MT–CO1 and MT–CO2 ) was quantified via quantitative RT-PCR; (D) Quantitation of mitochondrial SOD activity, wherein SOD activity decreased in ECHDC3 -knockdown cells. (E) <t>Mitophagy</t> biomarkers were detected via western blotting. β-Actin was used as a control. (F–I) Quantitation of the mitophagy pathway protein. Values were presented as mean ± standard error. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. CCCP: Carbonyl cyanide m-chlorophenyl hydrazone; ECHDC3 : Enoyl-CoA hydratase domain-containing protein 3; mtDNA: Mitochondrial DNA; RT-PCR: Real-time polymerase chain reaction; SOD: Superoxide dismutase; TMRE: Tetramethyl rhodamine ethyl ester.
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    Image Search Results


    Changes in mitochondrial function following ECHDC3 knockdown. (A) TMRE staining results based on ECHDC3 -knockdown cells. siNC cells emitted bright red-orange fluorescence. Cells treated with a mitochondrial membrane-potential disrupter, CCCP, showed very weak or complete absence of red-orange fluorescence. The average fluorescence intensity of the cells was calculated and quantitatively analyzed. (B–C) mtDNA copy number ( MT–CO1 and MT–CO2 ) was quantified via quantitative RT-PCR; (D) Quantitation of mitochondrial SOD activity, wherein SOD activity decreased in ECHDC3 -knockdown cells. (E) Mitophagy biomarkers were detected via western blotting. β-Actin was used as a control. (F–I) Quantitation of the mitophagy pathway protein. Values were presented as mean ± standard error. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. CCCP: Carbonyl cyanide m-chlorophenyl hydrazone; ECHDC3 : Enoyl-CoA hydratase domain-containing protein 3; mtDNA: Mitochondrial DNA; RT-PCR: Real-time polymerase chain reaction; SOD: Superoxide dismutase; TMRE: Tetramethyl rhodamine ethyl ester.

    Journal: Cancer Pathogenesis and Therapy

    Article Title: Metabolic pathways and chemotherapy resistance in acute myeloid leukemia (AML): Insights into Enoyl-CoA hydratase domain-containing protein 3 ( ECHDC3 ) as a potential therapeutic target

    doi: 10.1016/j.cpt.2025.08.002

    Figure Lengend Snippet: Changes in mitochondrial function following ECHDC3 knockdown. (A) TMRE staining results based on ECHDC3 -knockdown cells. siNC cells emitted bright red-orange fluorescence. Cells treated with a mitochondrial membrane-potential disrupter, CCCP, showed very weak or complete absence of red-orange fluorescence. The average fluorescence intensity of the cells was calculated and quantitatively analyzed. (B–C) mtDNA copy number ( MT–CO1 and MT–CO2 ) was quantified via quantitative RT-PCR; (D) Quantitation of mitochondrial SOD activity, wherein SOD activity decreased in ECHDC3 -knockdown cells. (E) Mitophagy biomarkers were detected via western blotting. β-Actin was used as a control. (F–I) Quantitation of the mitophagy pathway protein. Values were presented as mean ± standard error. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. CCCP: Carbonyl cyanide m-chlorophenyl hydrazone; ECHDC3 : Enoyl-CoA hydratase domain-containing protein 3; mtDNA: Mitochondrial DNA; RT-PCR: Real-time polymerase chain reaction; SOD: Superoxide dismutase; TMRE: Tetramethyl rhodamine ethyl ester.

    Article Snippet: Western blotting was performed to determine the expression of mitochondrial proteins, using the Mitophagy Antibody Sampler Kit (Cat# 43110, Cell Signaling Technology [CST], MA, USA) and an anti-β-actin mouse monoclonal antibody (Cat# 3700, CST, MA, USA).

    Techniques: Knockdown, Staining, Fluorescence, Membrane, Quantitative RT-PCR, Quantitation Assay, Activity Assay, Western Blot, Control, Reverse Transcription Polymerase Chain Reaction, Real-time Polymerase Chain Reaction

    High-glucose treatment affects mitochondrial morphology and mitochondrial dynamics in primary hepatocytes. A Morphological changes in the mitochondria of cells. Scale bar, 10 μm. B Intensity of mROS in cells. C Fluorescence photomicrograph of Tom20 examined in cells. Scale bar, 10 μm. D The expression of mitochondrial dynamics-related proteins (Tom20, Hsp60, and Drp1) in cells ( n = 3)

    Journal: Journal of Animal Science and Biotechnology

    Article Title: Mechanisms of high-glucose-induced mitochondrial damage and glycolipid accumulation in largemouth bass

    doi: 10.1186/s40104-025-01261-2

    Figure Lengend Snippet: High-glucose treatment affects mitochondrial morphology and mitochondrial dynamics in primary hepatocytes. A Morphological changes in the mitochondria of cells. Scale bar, 10 μm. B Intensity of mROS in cells. C Fluorescence photomicrograph of Tom20 examined in cells. Scale bar, 10 μm. D The expression of mitochondrial dynamics-related proteins (Tom20, Hsp60, and Drp1) in cells ( n = 3)

    Article Snippet: Tom20 , 1:1,000 , Cell Signaling Technology, #43110 T.

    Techniques: Fluorescence, Expressing

    High-glucose treatment affects mitochondrial morphology and mitochondrial dynamics in primary hepatocytes. A Morphological changes in the mitochondria of cells. Scale bar, 10 μm. B Intensity of mROS in cells. C Fluorescence photomicrograph of Tom20 examined in cells. Scale bar, 10 μm. D The expression of mitochondrial dynamics-related proteins (Tom20, Hsp60, and Drp1) in cells ( n = 3)

    Journal: Journal of Animal Science and Biotechnology

    Article Title: Mechanisms of high-glucose-induced mitochondrial damage and glycolipid accumulation in largemouth bass

    doi: 10.1186/s40104-025-01261-2

    Figure Lengend Snippet: High-glucose treatment affects mitochondrial morphology and mitochondrial dynamics in primary hepatocytes. A Morphological changes in the mitochondria of cells. Scale bar, 10 μm. B Intensity of mROS in cells. C Fluorescence photomicrograph of Tom20 examined in cells. Scale bar, 10 μm. D The expression of mitochondrial dynamics-related proteins (Tom20, Hsp60, and Drp1) in cells ( n = 3)

    Article Snippet: Drp1 , 1:1,000 , Cell Signaling Technology, #43110 T.

    Techniques: Fluorescence, Expressing