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coxiv polyclonal antibody  (Proteintech)


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    Proteintech coxiv polyclonal antibody
    Chymase reduces the metabolic activity and mitochondrial respiration of primary HLFs without affecting viability or mitochondrial protein abundance. ( A ) Oxygen consumption rate (OCR) profiles of primary HLFs, untreated or treated with 5 nM chymase for 24 h. Sequential injections include Oligomycin A (ATP synthase inhibitor), FCCP (protonophore), and a Rotenone/Antimycin A mixture (Complex I/III inhibitors). Data represent means ± SD. ( B ) Quantification of basal respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. * P < 0.1 (paired Student’s t-test). ( C ) Quantification of ATP-linked respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. ( D ) Quantification of maximal respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. ( E ) Extracellular acidification rate (ECAR) profiles of primary HLFs, untreated or treated with 5 nM chymase for 24 h. Sequential injections include Oligomycin A, FCCP, and a Rotenone/Antimycin A mixture (Complex I/III inhibitors). Data represent means ± SD. ( F ) Flow cytometric assessment of HLF viability and apoptosis after 24-hour treatment with 5 nM chymase, stained with Annexin V and DRAQ7. Populations include viable (Annexin V−/DRAQ7−), early apoptotic (Annexin V+/DRAQ7−), and late apoptotic/necrotic (Annexin V+/DRAQ7+) cells. Data are shown as means ± SEM. ( G ) Quantification of EdU-positive proliferating HLFs after 24-hour treatment with 5 nM chymase, relative to untreated cells. Data are presented as means ± SEM. ( H ) Quantification of HLF metabolic activity assessed by an independent PrestoBlue assay following 24-hour treatment with 5 nM chymase. Data are presented as means ± SEM. **** P ≤ 0.0001. ( I ) Representative Western blots showing the protein levels of subunits for oxidative phosphorylation (OXPHOS) complexes (Complex I, II, III, IV, V) in primary HLFs after 24-hour treatment with 5 nM chymase. ( J ) Total protein levels of <t>COXIV,</t> MTCO1, and MTCO2 are shown. GAPDH serves as a loading control
    Coxiv Polyclonal Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 552 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/coxiv+polyclonal+antibody/pmc12932338-34-5-1?v=Proteintech
    Average 96 stars, based on 552 article reviews
    coxiv polyclonal antibody - by Bioz Stars, 2026-08
    96/100 stars

    Images

    1) Product Images from "Mast Cell Chymase and Human Lung Fibroblast Interaction: Mechanisms and Implications for Asthma"

    Article Title: Mast Cell Chymase and Human Lung Fibroblast Interaction: Mechanisms and Implications for Asthma

    Journal: Inflammation

    doi: 10.1007/s10753-026-02460-3

    Chymase reduces the metabolic activity and mitochondrial respiration of primary HLFs without affecting viability or mitochondrial protein abundance. ( A ) Oxygen consumption rate (OCR) profiles of primary HLFs, untreated or treated with 5 nM chymase for 24 h. Sequential injections include Oligomycin A (ATP synthase inhibitor), FCCP (protonophore), and a Rotenone/Antimycin A mixture (Complex I/III inhibitors). Data represent means ± SD. ( B ) Quantification of basal respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. * P < 0.1 (paired Student’s t-test). ( C ) Quantification of ATP-linked respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. ( D ) Quantification of maximal respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. ( E ) Extracellular acidification rate (ECAR) profiles of primary HLFs, untreated or treated with 5 nM chymase for 24 h. Sequential injections include Oligomycin A, FCCP, and a Rotenone/Antimycin A mixture (Complex I/III inhibitors). Data represent means ± SD. ( F ) Flow cytometric assessment of HLF viability and apoptosis after 24-hour treatment with 5 nM chymase, stained with Annexin V and DRAQ7. Populations include viable (Annexin V−/DRAQ7−), early apoptotic (Annexin V+/DRAQ7−), and late apoptotic/necrotic (Annexin V+/DRAQ7+) cells. Data are shown as means ± SEM. ( G ) Quantification of EdU-positive proliferating HLFs after 24-hour treatment with 5 nM chymase, relative to untreated cells. Data are presented as means ± SEM. ( H ) Quantification of HLF metabolic activity assessed by an independent PrestoBlue assay following 24-hour treatment with 5 nM chymase. Data are presented as means ± SEM. **** P ≤ 0.0001. ( I ) Representative Western blots showing the protein levels of subunits for oxidative phosphorylation (OXPHOS) complexes (Complex I, II, III, IV, V) in primary HLFs after 24-hour treatment with 5 nM chymase. ( J ) Total protein levels of COXIV, MTCO1, and MTCO2 are shown. GAPDH serves as a loading control
    Figure Legend Snippet: Chymase reduces the metabolic activity and mitochondrial respiration of primary HLFs without affecting viability or mitochondrial protein abundance. ( A ) Oxygen consumption rate (OCR) profiles of primary HLFs, untreated or treated with 5 nM chymase for 24 h. Sequential injections include Oligomycin A (ATP synthase inhibitor), FCCP (protonophore), and a Rotenone/Antimycin A mixture (Complex I/III inhibitors). Data represent means ± SD. ( B ) Quantification of basal respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. * P < 0.1 (paired Student’s t-test). ( C ) Quantification of ATP-linked respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. ( D ) Quantification of maximal respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. ( E ) Extracellular acidification rate (ECAR) profiles of primary HLFs, untreated or treated with 5 nM chymase for 24 h. Sequential injections include Oligomycin A, FCCP, and a Rotenone/Antimycin A mixture (Complex I/III inhibitors). Data represent means ± SD. ( F ) Flow cytometric assessment of HLF viability and apoptosis after 24-hour treatment with 5 nM chymase, stained with Annexin V and DRAQ7. Populations include viable (Annexin V−/DRAQ7−), early apoptotic (Annexin V+/DRAQ7−), and late apoptotic/necrotic (Annexin V+/DRAQ7+) cells. Data are shown as means ± SEM. ( G ) Quantification of EdU-positive proliferating HLFs after 24-hour treatment with 5 nM chymase, relative to untreated cells. Data are presented as means ± SEM. ( H ) Quantification of HLF metabolic activity assessed by an independent PrestoBlue assay following 24-hour treatment with 5 nM chymase. Data are presented as means ± SEM. **** P ≤ 0.0001. ( I ) Representative Western blots showing the protein levels of subunits for oxidative phosphorylation (OXPHOS) complexes (Complex I, II, III, IV, V) in primary HLFs after 24-hour treatment with 5 nM chymase. ( J ) Total protein levels of COXIV, MTCO1, and MTCO2 are shown. GAPDH serves as a loading control

    Techniques Used: Activity Assay, Quantitative Proteomics, Staining, Prestoblue Assay, Western Blot, Phospho-proteomics, Control



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    Chymase reduces the metabolic activity and mitochondrial respiration of primary HLFs without affecting viability or mitochondrial protein abundance. ( A ) Oxygen consumption rate (OCR) profiles of primary HLFs, untreated or treated with 5 nM chymase for 24 h. Sequential injections include Oligomycin A (ATP synthase inhibitor), FCCP (protonophore), and a Rotenone/Antimycin A mixture (Complex I/III inhibitors). Data represent means ± SD. ( B ) Quantification of basal respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. * P < 0.1 (paired Student’s t-test). ( C ) Quantification of ATP-linked respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. ( D ) Quantification of maximal respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. ( E ) Extracellular acidification rate (ECAR) profiles of primary HLFs, untreated or treated with 5 nM chymase for 24 h. Sequential injections include Oligomycin A, FCCP, and a Rotenone/Antimycin A mixture (Complex I/III inhibitors). Data represent means ± SD. ( F ) Flow cytometric assessment of HLF viability and apoptosis after 24-hour treatment with 5 nM chymase, stained with Annexin V and DRAQ7. Populations include viable (Annexin V−/DRAQ7−), early apoptotic (Annexin V+/DRAQ7−), and late apoptotic/necrotic (Annexin V+/DRAQ7+) cells. Data are shown as means ± SEM. ( G ) Quantification of EdU-positive proliferating HLFs after 24-hour treatment with 5 nM chymase, relative to untreated cells. Data are presented as means ± SEM. ( H ) Quantification of HLF metabolic activity assessed by an independent PrestoBlue assay following 24-hour treatment with 5 nM chymase. Data are presented as means ± SEM. **** P ≤ 0.0001. ( I ) Representative Western blots showing the protein levels of subunits for oxidative phosphorylation (OXPHOS) complexes (Complex I, II, III, IV, V) in primary HLFs after 24-hour treatment with 5 nM chymase. ( J ) Total protein levels of <t>COXIV,</t> MTCO1, and MTCO2 are shown. GAPDH serves as a loading control
    Coxiv Polyclonal Antibody, 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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    Chymase reduces the metabolic activity and mitochondrial respiration of primary HLFs without affecting viability or mitochondrial protein abundance. ( A ) Oxygen consumption rate (OCR) profiles of primary HLFs, untreated or treated with 5 nM chymase for 24 h. Sequential injections include Oligomycin A (ATP synthase inhibitor), FCCP (protonophore), and a Rotenone/Antimycin A mixture (Complex I/III inhibitors). Data represent means ± SD. ( B ) Quantification of basal respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. * P < 0.1 (paired Student’s t-test). ( C ) Quantification of ATP-linked respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. ( D ) Quantification of maximal respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. ( E ) Extracellular acidification rate (ECAR) profiles of primary HLFs, untreated or treated with 5 nM chymase for 24 h. Sequential injections include Oligomycin A, FCCP, and a Rotenone/Antimycin A mixture (Complex I/III inhibitors). Data represent means ± SD. ( F ) Flow cytometric assessment of HLF viability and apoptosis after 24-hour treatment with 5 nM chymase, stained with Annexin V and DRAQ7. Populations include viable (Annexin V−/DRAQ7−), early apoptotic (Annexin V+/DRAQ7−), and late apoptotic/necrotic (Annexin V+/DRAQ7+) cells. Data are shown as means ± SEM. ( G ) Quantification of EdU-positive proliferating HLFs after 24-hour treatment with 5 nM chymase, relative to untreated cells. Data are presented as means ± SEM. ( H ) Quantification of HLF metabolic activity assessed by an independent PrestoBlue assay following 24-hour treatment with 5 nM chymase. Data are presented as means ± SEM. **** P ≤ 0.0001. ( I ) Representative Western blots showing the protein levels of subunits for oxidative phosphorylation (OXPHOS) complexes (Complex I, II, III, IV, V) in primary HLFs after 24-hour treatment with 5 nM chymase. ( J ) Total protein levels of <t>COXIV,</t> MTCO1, and MTCO2 are shown. GAPDH serves as a loading control
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    Image Search Results


    Chymase reduces the metabolic activity and mitochondrial respiration of primary HLFs without affecting viability or mitochondrial protein abundance. ( A ) Oxygen consumption rate (OCR) profiles of primary HLFs, untreated or treated with 5 nM chymase for 24 h. Sequential injections include Oligomycin A (ATP synthase inhibitor), FCCP (protonophore), and a Rotenone/Antimycin A mixture (Complex I/III inhibitors). Data represent means ± SD. ( B ) Quantification of basal respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. * P < 0.1 (paired Student’s t-test). ( C ) Quantification of ATP-linked respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. ( D ) Quantification of maximal respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. ( E ) Extracellular acidification rate (ECAR) profiles of primary HLFs, untreated or treated with 5 nM chymase for 24 h. Sequential injections include Oligomycin A, FCCP, and a Rotenone/Antimycin A mixture (Complex I/III inhibitors). Data represent means ± SD. ( F ) Flow cytometric assessment of HLF viability and apoptosis after 24-hour treatment with 5 nM chymase, stained with Annexin V and DRAQ7. Populations include viable (Annexin V−/DRAQ7−), early apoptotic (Annexin V+/DRAQ7−), and late apoptotic/necrotic (Annexin V+/DRAQ7+) cells. Data are shown as means ± SEM. ( G ) Quantification of EdU-positive proliferating HLFs after 24-hour treatment with 5 nM chymase, relative to untreated cells. Data are presented as means ± SEM. ( H ) Quantification of HLF metabolic activity assessed by an independent PrestoBlue assay following 24-hour treatment with 5 nM chymase. Data are presented as means ± SEM. **** P ≤ 0.0001. ( I ) Representative Western blots showing the protein levels of subunits for oxidative phosphorylation (OXPHOS) complexes (Complex I, II, III, IV, V) in primary HLFs after 24-hour treatment with 5 nM chymase. ( J ) Total protein levels of COXIV, MTCO1, and MTCO2 are shown. GAPDH serves as a loading control

    Journal: Inflammation

    Article Title: Mast Cell Chymase and Human Lung Fibroblast Interaction: Mechanisms and Implications for Asthma

    doi: 10.1007/s10753-026-02460-3

    Figure Lengend Snippet: Chymase reduces the metabolic activity and mitochondrial respiration of primary HLFs without affecting viability or mitochondrial protein abundance. ( A ) Oxygen consumption rate (OCR) profiles of primary HLFs, untreated or treated with 5 nM chymase for 24 h. Sequential injections include Oligomycin A (ATP synthase inhibitor), FCCP (protonophore), and a Rotenone/Antimycin A mixture (Complex I/III inhibitors). Data represent means ± SD. ( B ) Quantification of basal respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. * P < 0.1 (paired Student’s t-test). ( C ) Quantification of ATP-linked respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. ( D ) Quantification of maximal respiration in HLFs following 24-hour treatment with 5 nM chymase. Data are presented as means + SD, pooled from three independent experiments. ( E ) Extracellular acidification rate (ECAR) profiles of primary HLFs, untreated or treated with 5 nM chymase for 24 h. Sequential injections include Oligomycin A, FCCP, and a Rotenone/Antimycin A mixture (Complex I/III inhibitors). Data represent means ± SD. ( F ) Flow cytometric assessment of HLF viability and apoptosis after 24-hour treatment with 5 nM chymase, stained with Annexin V and DRAQ7. Populations include viable (Annexin V−/DRAQ7−), early apoptotic (Annexin V+/DRAQ7−), and late apoptotic/necrotic (Annexin V+/DRAQ7+) cells. Data are shown as means ± SEM. ( G ) Quantification of EdU-positive proliferating HLFs after 24-hour treatment with 5 nM chymase, relative to untreated cells. Data are presented as means ± SEM. ( H ) Quantification of HLF metabolic activity assessed by an independent PrestoBlue assay following 24-hour treatment with 5 nM chymase. Data are presented as means ± SEM. **** P ≤ 0.0001. ( I ) Representative Western blots showing the protein levels of subunits for oxidative phosphorylation (OXPHOS) complexes (Complex I, II, III, IV, V) in primary HLFs after 24-hour treatment with 5 nM chymase. ( J ) Total protein levels of COXIV, MTCO1, and MTCO2 are shown. GAPDH serves as a loading control

    Article Snippet: From Proteintech (Rosemont, IL, USA): COXIV Polyclonal antibody (1:5000, #11242-1-AP).

    Techniques: Activity Assay, Quantitative Proteomics, Staining, Prestoblue Assay, Western Blot, Phospho-proteomics, Control

    a Confocal fluorescence images of HeLa cells transfected without (Blank), and with 180 nM CD63APT-TPP, OK-MLIR and OK-MLIR in presence of 10-min UV irradiation. Scale bar: 30 µm. MitoRed, LysoBlue and FAM were excited with 579, 373 and 494 nm lasers, respectively. b Pearson Correlation analysis of ( a ) by investigating the fluorescence signals of MitoRed and LysoBlue. Shown are mean ± SEM from ten individual cells. (Blank vs CD63APT-TPP, P = 5.45 × 10 −16 and OK-MLIR vs OK-MLIR (UV), P = 3.00 × 10 −11 , **** P < 0.0001, two-tailed Student’s t test). c Super-resolution images of HeLa cells transfected without (Blank), and with 180 nM CD63APT-TPP, OK-MLIR and OK-MLIR in presence of 10-min UV irradiation. MitoTracker Green and LysoTracker were excited with 490 and 580 nm lasers, respectively. Scale bar: 10 µm. d TEM images of HeLa cells (Blank) and HeLa cells treated with 180 nM CD63APT-TPP, OK-MLIR and OK-MLIR in presence of 10-min UV irradiation. Scale bar: 5 µm. e Confocal images of HeLa cells (Blank) and HeLa cells treated with 180 nM CD63APT-TPP, OK-MLIR, and OK-MLIR in presence of 10-min UV irradiation. MtphagyDye, LysoDye and MitoBright DeepRed were used for staining mitochondrial autophagy, lysosomes, and mitochondria, respectively. Scale bar: 50 µm. f Confocal immunofluorescence staining images of HeLa cells treated without (Blank) and with 180 nM CD63APT-TPP, OK-MLIR and OK-MLIR in presence of 10-min UV irradiation., then labeled with COXIV antibody (green) and DAPI (blue). Scale bar: 100 µm. g Corresponding green fluorescence intensities were extracted from ( f ) for quantitative analysis. Shown are mean ± SEM from ten individual cells. (Blank vs CD63APT-TPP, P = 6.70 × 10 −9 and OK-MLIR vs OK-MLIR (UV), P = 7.31 × 10 −7 , **** P < 0.0001, two-tailed Student’s t test). h Western blo t map of TOMM20 protein in HeLa cells treated without (Lane 1) and with CD63APT-TPP (2), OK-MLIR (3), and OK-MLIR in presence of 10-min UV irradiation (4). Image representation of 3 experiments. Source data are provided as a file.

    Journal: Nature Communications

    Article Title: Dual-key cooperatively activated DNA regulator for controlling mitochondria-lysosome interactions

    doi: 10.1038/s41467-025-63040-x

    Figure Lengend Snippet: a Confocal fluorescence images of HeLa cells transfected without (Blank), and with 180 nM CD63APT-TPP, OK-MLIR and OK-MLIR in presence of 10-min UV irradiation. Scale bar: 30 µm. MitoRed, LysoBlue and FAM were excited with 579, 373 and 494 nm lasers, respectively. b Pearson Correlation analysis of ( a ) by investigating the fluorescence signals of MitoRed and LysoBlue. Shown are mean ± SEM from ten individual cells. (Blank vs CD63APT-TPP, P = 5.45 × 10 −16 and OK-MLIR vs OK-MLIR (UV), P = 3.00 × 10 −11 , **** P < 0.0001, two-tailed Student’s t test). c Super-resolution images of HeLa cells transfected without (Blank), and with 180 nM CD63APT-TPP, OK-MLIR and OK-MLIR in presence of 10-min UV irradiation. MitoTracker Green and LysoTracker were excited with 490 and 580 nm lasers, respectively. Scale bar: 10 µm. d TEM images of HeLa cells (Blank) and HeLa cells treated with 180 nM CD63APT-TPP, OK-MLIR and OK-MLIR in presence of 10-min UV irradiation. Scale bar: 5 µm. e Confocal images of HeLa cells (Blank) and HeLa cells treated with 180 nM CD63APT-TPP, OK-MLIR, and OK-MLIR in presence of 10-min UV irradiation. MtphagyDye, LysoDye and MitoBright DeepRed were used for staining mitochondrial autophagy, lysosomes, and mitochondria, respectively. Scale bar: 50 µm. f Confocal immunofluorescence staining images of HeLa cells treated without (Blank) and with 180 nM CD63APT-TPP, OK-MLIR and OK-MLIR in presence of 10-min UV irradiation., then labeled with COXIV antibody (green) and DAPI (blue). Scale bar: 100 µm. g Corresponding green fluorescence intensities were extracted from ( f ) for quantitative analysis. Shown are mean ± SEM from ten individual cells. (Blank vs CD63APT-TPP, P = 6.70 × 10 −9 and OK-MLIR vs OK-MLIR (UV), P = 7.31 × 10 −7 , **** P < 0.0001, two-tailed Student’s t test). h Western blo t map of TOMM20 protein in HeLa cells treated without (Lane 1) and with CD63APT-TPP (2), OK-MLIR (3), and OK-MLIR in presence of 10-min UV irradiation (4). Image representation of 3 experiments. Source data are provided as a file.

    Article Snippet: COXIV polyclonal antibody was purchased from Sanying Biotechnology Co., LTD. (Wuhan, China).

    Techniques: Fluorescence, Transfection, Irradiation, Two Tailed Test, Staining, Immunofluorescence, Labeling, Western Blot

    a Schematic illustration of the structure and dual keys triggered DK-MLIR activation for mitochondrial binding. b Confocal images of lysosomes (LysoTracker) and mitochondria (MitoTracker Green) in HeLa cells treated without (Blank) and with 180 nM DK-MLIR (the DK-MLIR row), 180 nM DK-MLIR in presence of 100 µM BSO and 10-min UV irradiation (BSO + UV), 180 nM DK-MLIR in presence of 100 µM BSO (BSO), and DK-MLIR in presence of 10-min UV irradiation (UV). MitoTracker Green and LysoTracker were excited with 490 and 580 nm lasers, respectively. Scale bar: 50 µm. c Pearson Correlation analysis was performed on the red and green fluorescence in ( b ). Shown are mean ± SEM from ten individual cells. (Blank vs UV, P = 1.72 × 10 −13 , **** P < 0.0001, two-tailed Student’s t test). d Confocal immunofluorescence images of HeLa cells treated without (Blank) and with 180 nM DK-MLIR (DK-MLIR), 180 nM DK-MLIR in presence of 100 µM BSO and 10-min UV irradiation (BSO + UV), 180 nM DK-MLIR in presence of 100 µM BSO (BSO), and DK-MLIR in presence of 10-min UV irradiation (UV); and then labeled with COXIV antibody (green) and DAPI (blue). Scale bar: 60 µm. e Green fluorescence intensity was extracted from ( d ) for quantitative analysis. Shown are mean ± SEM from ten individual cells. (Blank vs UV, P = 6.90 × 10 −16 , **** P < 0.0001, two-tailed Student’s t test). f Western Blot map of TOMM20 and COXIV proteins in HeLa cells treated with 180 nM DK-MLIR in presence of 100 µM BSO (Lane 1), 180 nM DK-MLIR (2), 180 nM DK-MLIR in presence of 10-min UV irradiation (3), and 180 nM DK-MLIR in presence of 100 µM BSO and 10-min UV irradiation (4). Image representation of 3 experiments. Source data are provided as a file.

    Journal: Nature Communications

    Article Title: Dual-key cooperatively activated DNA regulator for controlling mitochondria-lysosome interactions

    doi: 10.1038/s41467-025-63040-x

    Figure Lengend Snippet: a Schematic illustration of the structure and dual keys triggered DK-MLIR activation for mitochondrial binding. b Confocal images of lysosomes (LysoTracker) and mitochondria (MitoTracker Green) in HeLa cells treated without (Blank) and with 180 nM DK-MLIR (the DK-MLIR row), 180 nM DK-MLIR in presence of 100 µM BSO and 10-min UV irradiation (BSO + UV), 180 nM DK-MLIR in presence of 100 µM BSO (BSO), and DK-MLIR in presence of 10-min UV irradiation (UV). MitoTracker Green and LysoTracker were excited with 490 and 580 nm lasers, respectively. Scale bar: 50 µm. c Pearson Correlation analysis was performed on the red and green fluorescence in ( b ). Shown are mean ± SEM from ten individual cells. (Blank vs UV, P = 1.72 × 10 −13 , **** P < 0.0001, two-tailed Student’s t test). d Confocal immunofluorescence images of HeLa cells treated without (Blank) and with 180 nM DK-MLIR (DK-MLIR), 180 nM DK-MLIR in presence of 100 µM BSO and 10-min UV irradiation (BSO + UV), 180 nM DK-MLIR in presence of 100 µM BSO (BSO), and DK-MLIR in presence of 10-min UV irradiation (UV); and then labeled with COXIV antibody (green) and DAPI (blue). Scale bar: 60 µm. e Green fluorescence intensity was extracted from ( d ) for quantitative analysis. Shown are mean ± SEM from ten individual cells. (Blank vs UV, P = 6.90 × 10 −16 , **** P < 0.0001, two-tailed Student’s t test). f Western Blot map of TOMM20 and COXIV proteins in HeLa cells treated with 180 nM DK-MLIR in presence of 100 µM BSO (Lane 1), 180 nM DK-MLIR (2), 180 nM DK-MLIR in presence of 10-min UV irradiation (3), and 180 nM DK-MLIR in presence of 100 µM BSO and 10-min UV irradiation (4). Image representation of 3 experiments. Source data are provided as a file.

    Article Snippet: COXIV polyclonal antibody was purchased from Sanying Biotechnology Co., LTD. (Wuhan, China).

    Techniques: Activation Assay, Binding Assay, Irradiation, Fluorescence, Two Tailed Test, Immunofluorescence, Labeling, Western Blot

    TJ0113 selectively induces mitophagy through PINK1–Parkin pathway. (A) Molecular structure of TJ0113. (B, C) Western blot analysis of autophagy (LC3B, p62) and mitochondrial proteins (COXIV, TOM20) in HEK293T cells treated with TJ0113 and/or CCCP. (D) JC-1 staining shows mitochondrial membrane potential of HEK293T cells. (E) Relative mRNA levels of PINK1 , PARKIN , BNIP3 , and FUNDC1 in HEK293T cells. (F, G) Western blotting of phosphorylated PINK1 (p-PINK1) using samples from panel (B, C) . The β-actin was reused due to identical sample sets. β-actin served as loading control. Data: mean ± SEM, n=3. ns, not significant; *P<0.05; **P<0.01; ***P<0.001; ****P<0.0001. (D, E) Ordinary one-way ANOVA with Tukey’s multiple comparisons test.

    Journal: Frontiers in Pharmacology

    Article Title: Novel mitophagy inducer TJ0113 alleviates pulmonary inflammation during acute lung injury

    doi: 10.3389/fphar.2025.1590458

    Figure Lengend Snippet: TJ0113 selectively induces mitophagy through PINK1–Parkin pathway. (A) Molecular structure of TJ0113. (B, C) Western blot analysis of autophagy (LC3B, p62) and mitochondrial proteins (COXIV, TOM20) in HEK293T cells treated with TJ0113 and/or CCCP. (D) JC-1 staining shows mitochondrial membrane potential of HEK293T cells. (E) Relative mRNA levels of PINK1 , PARKIN , BNIP3 , and FUNDC1 in HEK293T cells. (F, G) Western blotting of phosphorylated PINK1 (p-PINK1) using samples from panel (B, C) . The β-actin was reused due to identical sample sets. β-actin served as loading control. Data: mean ± SEM, n=3. ns, not significant; *P<0.05; **P<0.01; ***P<0.001; ****P<0.0001. (D, E) Ordinary one-way ANOVA with Tukey’s multiple comparisons test.

    Article Snippet: The primary antibodies used include: LC3B rabbit polyclonal antibody (Abcam, ab168831), β-actin mouse monoclonal antibody (Cell Signaling Technology, 3700), P-IKK α/β rabbit monoclonal antibody (Cell Signaling Technology, 2697), P-IκBα rabbit monoclonal antibody (Cell Signaling Technology, 2859), p-p65 rabbit monoclonal antibody (Cell Signaling Technology, 3033), p65 rabbit monoclonal antibody (Cell Signaling Technology, 8242), IκBα rabbit polyclonal antibody (Cell Signaling Technology, 9242), p62 rabbit polyclonal antibody (Cell Signaling Technology, 5114), IKKα/β rabbit monoclonal antibody (Cell Signaling Technology, 2697), COXIV rabbit polyclonal antibody (Cell Signaling Technology, 4850), TOM20 mouse monoclonal antibody (Santa Cruz, sc-17764), p-PINK1 rabbit polyclonal antibody (Signalway Antibody, 29297), NLRP3 mouse monoclonal antibody (AdipoGen, AG-20B-0014), Total and Cleaved IL-1β Antibody (Abmart, P50520-1R1S), and caspase-1 rabbit polyclonal antibody (Proteintech, 22915-1-AP).

    Techniques: Western Blot, Staining, Membrane, Control