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cytochrome c oxidase subunit 4  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cytochrome c oxidase subunit 4
    Voluntary exercise alters left ventricle gene and protein expression related to mitochondrial biogenesis and dynamics in high fat- and chow-fed mice. (A) Western blot analysis to assess purity of crude mitochondria isolation where left ventricle mitochondrial pellet expresses mitochondrial marker TOM70 and COXIV and supernatant expresses calnexin. Protein expression of (B) LCLAT1 and (C) MFN2 in left ventricle-isolated crude mitochondria and (D) LCLAT1, (E) PGC-1α, and (F) MFN2 in left ventricle tissue from male VET or sedentary mice fed an HFD or chow diet. Left ventricle mRNA expression of (G) OPA1 and (H) DRP1 in male VET or sedentary mice fed an HFD or chow diet. Values were calculated relative to 18S housekeeper. Calnexin and β-actin were used as internal controls of protein loading in left ventricle samples and COXIV as internal control of protein loading in crude mitochondria samples. Analysis was performed using two-way analysis of variance with Tukey’s post hoc test for multiple comparisons. Data are expressed as mean ± standard error of the mean. (B–C) n : 5–6 per group. (D–F) n = 7 per group. (G and H) n = 9 per group. CE = chow exercise; CS = chow sedentary; COXIV = cytochrome c oxidase subunit 4; DRP1 = dynamin-related protein 1; HE = high fat diet exercise; HFD = high fat diet; HS = high fat diet sedentary; LCLAT1 = lysocardiolipin acyltransferase 1; MFN2 = mitofusin-2; OPA1 = optic atrophy 1; PGC-1α = peroxisome proliferator-activated receptor gamma coactivator-1α; TOM70 = translocase of outer mitochondria membrane 70; VET = voluntary exercise training.
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    Images

    1) Product Images from "Influence of diet-induced obesity and voluntary exercise training on cardiac lipids and mitochondrial function in mice"

    Article Title: Influence of diet-induced obesity and voluntary exercise training on cardiac lipids and mitochondrial function in mice

    Journal: Journal of Sport and Health Science

    doi: 10.1016/j.jshs.2025.101095

    Voluntary exercise alters left ventricle gene and protein expression related to mitochondrial biogenesis and dynamics in high fat- and chow-fed mice. (A) Western blot analysis to assess purity of crude mitochondria isolation where left ventricle mitochondrial pellet expresses mitochondrial marker TOM70 and COXIV and supernatant expresses calnexin. Protein expression of (B) LCLAT1 and (C) MFN2 in left ventricle-isolated crude mitochondria and (D) LCLAT1, (E) PGC-1α, and (F) MFN2 in left ventricle tissue from male VET or sedentary mice fed an HFD or chow diet. Left ventricle mRNA expression of (G) OPA1 and (H) DRP1 in male VET or sedentary mice fed an HFD or chow diet. Values were calculated relative to 18S housekeeper. Calnexin and β-actin were used as internal controls of protein loading in left ventricle samples and COXIV as internal control of protein loading in crude mitochondria samples. Analysis was performed using two-way analysis of variance with Tukey’s post hoc test for multiple comparisons. Data are expressed as mean ± standard error of the mean. (B–C) n : 5–6 per group. (D–F) n = 7 per group. (G and H) n = 9 per group. CE = chow exercise; CS = chow sedentary; COXIV = cytochrome c oxidase subunit 4; DRP1 = dynamin-related protein 1; HE = high fat diet exercise; HFD = high fat diet; HS = high fat diet sedentary; LCLAT1 = lysocardiolipin acyltransferase 1; MFN2 = mitofusin-2; OPA1 = optic atrophy 1; PGC-1α = peroxisome proliferator-activated receptor gamma coactivator-1α; TOM70 = translocase of outer mitochondria membrane 70; VET = voluntary exercise training.
    Figure Legend Snippet: Voluntary exercise alters left ventricle gene and protein expression related to mitochondrial biogenesis and dynamics in high fat- and chow-fed mice. (A) Western blot analysis to assess purity of crude mitochondria isolation where left ventricle mitochondrial pellet expresses mitochondrial marker TOM70 and COXIV and supernatant expresses calnexin. Protein expression of (B) LCLAT1 and (C) MFN2 in left ventricle-isolated crude mitochondria and (D) LCLAT1, (E) PGC-1α, and (F) MFN2 in left ventricle tissue from male VET or sedentary mice fed an HFD or chow diet. Left ventricle mRNA expression of (G) OPA1 and (H) DRP1 in male VET or sedentary mice fed an HFD or chow diet. Values were calculated relative to 18S housekeeper. Calnexin and β-actin were used as internal controls of protein loading in left ventricle samples and COXIV as internal control of protein loading in crude mitochondria samples. Analysis was performed using two-way analysis of variance with Tukey’s post hoc test for multiple comparisons. Data are expressed as mean ± standard error of the mean. (B–C) n : 5–6 per group. (D–F) n = 7 per group. (G and H) n = 9 per group. CE = chow exercise; CS = chow sedentary; COXIV = cytochrome c oxidase subunit 4; DRP1 = dynamin-related protein 1; HE = high fat diet exercise; HFD = high fat diet; HS = high fat diet sedentary; LCLAT1 = lysocardiolipin acyltransferase 1; MFN2 = mitofusin-2; OPA1 = optic atrophy 1; PGC-1α = peroxisome proliferator-activated receptor gamma coactivator-1α; TOM70 = translocase of outer mitochondria membrane 70; VET = voluntary exercise training.

    Techniques Used: Expressing, Western Blot, Isolation, Marker, Control, Membrane

    Related Articles

    Incubation:

    Article Title: Modulating Subcellular Localization to Preserve the Stability and Functionality of Intracellular Nanobodies
    Article Snippet: .. Following permeabilization with 0.1% Triton X-100 in PBS for 5 min at room temperature and three PBS washes, cells were blocked with 5% BSA in PBS for 1 h at room temperature before overnight incubation at 4 °C with primary antibodies diluted in 5% BSA/PBS: anti-Calreticulin (ER marker, 1:400; #ab92516, Abcam, Cambridge, MA, USA), anti-COX IV (mitochondrial outer membrane, 1:200; #4850T, CST, Danvers, MA, USA), anti-Ras (membrane system, 1:200; CST #91054S), anti-FLAG (1:400; Sigma #F1804), and anti-STAT3 (1:800; CST #12640s). .. After three PBS washes, cells were incubated for 1 h at room temperature with secondary antibodies: CoraLite488-conjugated goat anti-rabbit IgG (1:200; #SA00013-2, Proteintech, Wuhan, China), CoraLite Plus 594-conjugated goat anti-mouse IgG (1:200; #RGAM004, Proteintech, Wuhan, China), and CoraLite488-conjugated goat anti-mouse IgG (1:200; #SA00013-1, Proteintech, Wuhan, China), followed by nuclear staining with DAPI (1:1000; #C1002, Beyotime Shanghai, China) and F-actin staining with fluorescein phalloidin (1:1000; #HY-K0902, MedChemExpress, Monmouth Junction, NJ, USA).

    Article Title: Decidual protein induced by progesterone enhances HIF-1α stability to promote mitophagy and glycolysis.
    Article Snippet: doi:10.1111/febs.70489 Mitophagy, the process of removing mitochondria through the autophagy– lysosome pathway, is crucial for maintaining cellular homeostasis.. However, its regulatory mechanisms and pathological implications remain poorly understood.. In our study, we revealed that decidual protein induced by progesterone (DEPP) plays a significant role in mitophagy through the DEPP–HIF-1a–BNIP3/NIX axis.

    Marker:

    Article Title: Modulating Subcellular Localization to Preserve the Stability and Functionality of Intracellular Nanobodies
    Article Snippet: .. Following permeabilization with 0.1% Triton X-100 in PBS for 5 min at room temperature and three PBS washes, cells were blocked with 5% BSA in PBS for 1 h at room temperature before overnight incubation at 4 °C with primary antibodies diluted in 5% BSA/PBS: anti-Calreticulin (ER marker, 1:400; #ab92516, Abcam, Cambridge, MA, USA), anti-COX IV (mitochondrial outer membrane, 1:200; #4850T, CST, Danvers, MA, USA), anti-Ras (membrane system, 1:200; CST #91054S), anti-FLAG (1:400; Sigma #F1804), and anti-STAT3 (1:800; CST #12640s). .. After three PBS washes, cells were incubated for 1 h at room temperature with secondary antibodies: CoraLite488-conjugated goat anti-rabbit IgG (1:200; #SA00013-2, Proteintech, Wuhan, China), CoraLite Plus 594-conjugated goat anti-mouse IgG (1:200; #RGAM004, Proteintech, Wuhan, China), and CoraLite488-conjugated goat anti-mouse IgG (1:200; #SA00013-1, Proteintech, Wuhan, China), followed by nuclear staining with DAPI (1:1000; #C1002, Beyotime Shanghai, China) and F-actin staining with fluorescein phalloidin (1:1000; #HY-K0902, MedChemExpress, Monmouth Junction, NJ, USA).

    Membrane:

    Article Title: Modulating Subcellular Localization to Preserve the Stability and Functionality of Intracellular Nanobodies
    Article Snippet: .. Following permeabilization with 0.1% Triton X-100 in PBS for 5 min at room temperature and three PBS washes, cells were blocked with 5% BSA in PBS for 1 h at room temperature before overnight incubation at 4 °C with primary antibodies diluted in 5% BSA/PBS: anti-Calreticulin (ER marker, 1:400; #ab92516, Abcam, Cambridge, MA, USA), anti-COX IV (mitochondrial outer membrane, 1:200; #4850T, CST, Danvers, MA, USA), anti-Ras (membrane system, 1:200; CST #91054S), anti-FLAG (1:400; Sigma #F1804), and anti-STAT3 (1:800; CST #12640s). .. After three PBS washes, cells were incubated for 1 h at room temperature with secondary antibodies: CoraLite488-conjugated goat anti-rabbit IgG (1:200; #SA00013-2, Proteintech, Wuhan, China), CoraLite Plus 594-conjugated goat anti-mouse IgG (1:200; #RGAM004, Proteintech, Wuhan, China), and CoraLite488-conjugated goat anti-mouse IgG (1:200; #SA00013-1, Proteintech, Wuhan, China), followed by nuclear staining with DAPI (1:1000; #C1002, Beyotime Shanghai, China) and F-actin staining with fluorescein phalloidin (1:1000; #HY-K0902, MedChemExpress, Monmouth Junction, NJ, USA).

    Electrochemiluminescence:

    Article Title: Decidual protein induced by progesterone enhances HIF-1α stability to promote mitophagy and glycolysis.
    Article Snippet: doi:10.1111/febs.70489 Mitophagy, the process of removing mitochondria through the autophagy– lysosome pathway, is crucial for maintaining cellular homeostasis.. However, its regulatory mechanisms and pathological implications remain poorly understood.. In our study, we revealed that decidual protein induced by progesterone (DEPP) plays a significant role in mitophagy through the DEPP–HIF-1a–BNIP3/NIX axis.

    Protein Concentration:

    Article Title: Decidual protein induced by progesterone enhances HIF-1α stability to promote mitophagy and glycolysis.
    Article Snippet: doi:10.1111/febs.70489 Mitophagy, the process of removing mitochondria through the autophagy– lysosome pathway, is crucial for maintaining cellular homeostasis.. However, its regulatory mechanisms and pathological implications remain poorly understood.. In our study, we revealed that decidual protein induced by progesterone (DEPP) plays a significant role in mitophagy through the DEPP–HIF-1a–BNIP3/NIX axis.

    Western Blot:

    Article Title: FAK modulates glioblastoma stem cell energetics via regulation of glycolysis and glutamine oxidation
    Article Snippet: .. Antibodies used for western blotting were anti-FAK (Cell Signaling Technology; #3285, 1:1000), anti-Phospho-FAK (Tyr397) (Cell Signaling Technology; #3283, 1:1000), anti-NF1 (Bethyl; #A300-140A, 1:2000), anti-PTEN (Cell Signaling Technology; #9559, 1:1000), anti-EGFR (Cell Signaling Technology; #4267, 1:1000), anti-COX IV (Cell Signaling Technology; #4850, 1:1000), anti-cofilin (Cell Signaling Technology; #5175, 1:1000), anti-Glut1 (Cell Signaling Technology; #73015, 1:1000), anti-Enolase 2 (Cell Signaling Technology; #24330, 1:1000). .. Antibodies used for western blotting were anti-FAK (Cell Signaling Technology; #3285, 1:1000), anti-Phospho-FAK (Tyr397) (Cell Signaling Technology; #3283, 1:1000), anti-NF1 (Bethyl; #A300-140A, 1:2000), anti-PTEN (Cell Signaling Technology; #9559, 1:1000), anti-EGFR (Cell Signaling Technology; #4267, 1:1000), anti-COX IV (Cell Signaling Technology; #4850, 1:1000), anti-cofilin (Cell Signaling Technology; #5175, 1:1000), anti-Glut1 (Cell Signaling Technology; #73015, 1:1000), anti-Enolase 2 (Cell Signaling Technology; #24330, 1:1000).

    Article Title: FAK modulates glioblastoma stem cell energetics via regulation of glycolysis and glutamine oxidation.
    Article Snippet: .. Antibodies used for western blotting were anti-FAK (Cell Signaling Technology; #3285, 1:1000), anti-Phospho-FAK (Tyr397) (Cell Signalling Technology; #3283, 1:1000), anti-NF1 (Bethyl; #A300-140A, 1:2000), anti-PTEN (Cell Signalling Technology; #9559, 1:1000), antiEGFR (Cell Signalling Technology; #4267, 1:1000), anti-COX IV (Cell Signaling Technology; #4850, 1:1000), anti- COFILIN (Cell Signaling Technology; #5175, 1:1000), anti-Glut1 (Cell Signalling Technology;# 73015, 1:1000), anti-Enolase 2 (Cell Signaling Technology; #24330, 1:1000). .. Antibodies used for western blotting were anti-FAK (Cell Signaling Technology; #3285, 1:1000), anti-Phospho-FAK (Tyr397) (Cell Signalling Technology; #3283, 1:1000), anti-NF1 (Bethyl; #A300-140A, 1:2000), anti-PTEN (Cell Signalling Technology; #9559, 1:1000), antiEGFR (Cell Signalling Technology; #4267, 1:1000), anti-COX IV (Cell Signaling Technology; #4850, 1:1000), anti- COFILIN (Cell Signaling Technology; #5175, 1:1000), anti-Glut1 (Cell Signalling Technology;# 73015, 1:1000), anti-Enolase 2 (Cell Signaling Technology; #24330, 1:1000).



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    Voluntary exercise alters left ventricle gene and protein expression related to mitochondrial biogenesis and dynamics in high fat- and chow-fed mice. (A) Western blot analysis to assess purity of crude mitochondria isolation where left ventricle mitochondrial pellet expresses mitochondrial marker TOM70 and COXIV and supernatant expresses calnexin. Protein expression of (B) LCLAT1 and (C) MFN2 in left ventricle-isolated crude mitochondria and (D) LCLAT1, (E) PGC-1α, and (F) MFN2 in left ventricle tissue from male VET or sedentary mice fed an HFD or chow diet. Left ventricle mRNA expression of (G) OPA1 and (H) DRP1 in male VET or sedentary mice fed an HFD or chow diet. Values were calculated relative to 18S housekeeper. Calnexin and β-actin were used as internal controls of protein loading in left ventricle samples and COXIV as internal control of protein loading in crude mitochondria samples. Analysis was performed using two-way analysis of variance with Tukey’s post hoc test for multiple comparisons. Data are expressed as mean ± standard error of the mean. (B–C) n : 5–6 per group. (D–F) n = 7 per group. (G and H) n = 9 per group. CE = chow exercise; CS = chow sedentary; COXIV = cytochrome c oxidase subunit 4; DRP1 = dynamin-related protein 1; HE = high fat diet exercise; HFD = high fat diet; HS = high fat diet sedentary; LCLAT1 = lysocardiolipin acyltransferase 1; MFN2 = mitofusin-2; OPA1 = optic atrophy 1; PGC-1α = peroxisome proliferator-activated receptor gamma coactivator-1α; TOM70 = translocase of outer mitochondria membrane 70; VET = voluntary exercise training.

    Journal: Journal of Sport and Health Science

    Article Title: Influence of diet-induced obesity and voluntary exercise training on cardiac lipids and mitochondrial function in mice

    doi: 10.1016/j.jshs.2025.101095

    Figure Lengend Snippet: Voluntary exercise alters left ventricle gene and protein expression related to mitochondrial biogenesis and dynamics in high fat- and chow-fed mice. (A) Western blot analysis to assess purity of crude mitochondria isolation where left ventricle mitochondrial pellet expresses mitochondrial marker TOM70 and COXIV and supernatant expresses calnexin. Protein expression of (B) LCLAT1 and (C) MFN2 in left ventricle-isolated crude mitochondria and (D) LCLAT1, (E) PGC-1α, and (F) MFN2 in left ventricle tissue from male VET or sedentary mice fed an HFD or chow diet. Left ventricle mRNA expression of (G) OPA1 and (H) DRP1 in male VET or sedentary mice fed an HFD or chow diet. Values were calculated relative to 18S housekeeper. Calnexin and β-actin were used as internal controls of protein loading in left ventricle samples and COXIV as internal control of protein loading in crude mitochondria samples. Analysis was performed using two-way analysis of variance with Tukey’s post hoc test for multiple comparisons. Data are expressed as mean ± standard error of the mean. (B–C) n : 5–6 per group. (D–F) n = 7 per group. (G and H) n = 9 per group. CE = chow exercise; CS = chow sedentary; COXIV = cytochrome c oxidase subunit 4; DRP1 = dynamin-related protein 1; HE = high fat diet exercise; HFD = high fat diet; HS = high fat diet sedentary; LCLAT1 = lysocardiolipin acyltransferase 1; MFN2 = mitofusin-2; OPA1 = optic atrophy 1; PGC-1α = peroxisome proliferator-activated receptor gamma coactivator-1α; TOM70 = translocase of outer mitochondria membrane 70; VET = voluntary exercise training.

    Article Snippet: Immunoblotting was performed with antibodies against lysocardiolipin acyltransferase 1(LCLAT1, PA5-25627; Thermo Fisher Scientific), PGC-1α (ab191838; Abcam, Cambridge, UK), MFN2 (PA5-118059; Thermo Fisher Scientific), ANP (sc-18811; Santa Cruz, Dallas, TX, USA), tumor necrosis factor alpha (TNFα, 3707; Cell Signaling, Danvers, MA, USA), phosphorylated adenosine monophosphate-activated protein kinase (AMPK, 2531; Cell Signaling), AMPKα (2532; Cell Signaling), Perilipin 5 (PA1-46215; Thermo Fisher Scientific), translocase of outer mitochondria membrane 70 (TOM70, 65675; Cell Signaling), cytochrome c oxidase subunit 4 (COXIV, 4844; Cell Signaling), and calnexin (208880; Merck, Rahway, NJ, USA).

    Techniques: Expressing, Western Blot, Isolation, Marker, Control, Membrane

    a Diagram of lipolysis in an adipocyte in WT mice and Pnpla2 –/– mice. Pnpla2 encodes ATGL, a key intracellular lipase involved in the hydrolysis of stored fat and FFA release. Pnpla2 –/– mice are not able to liberate FFAs from adipose TG depots. b Weight quantification of BAT and WAT in WT mice and Pnpla2 –/– mice under 30 °C or 4 °C ( n = 4 samples per group). c Histological analysis of BAT and WAT in WT mice and Pnpla2 –/– mice under 30 °C or 4 °C. Quantification of adipocyte size ( n = 8 random fields per group). Scale bar: 100 μm. d Immunohistochemical staining of BAT and WAT with UCP1 and COX4, followed by counterstaining with DAPI (blue) in WT mice and Pnpla2 –/– mice under 30 °C or 4 °C. Quantification of UCP1 + signals and COX4 + signals ( n = 8 random fields per group). Scale bar: 50 μm. e c-FFA levels in WT mice and Pnpla2 –/– mice under 30 °C or 4 °C ( n = 4 mice per group). f PLT, PDW, and MPV analysis in PB from WT mice and Pnpla2 –/– mice under 30 °C or 4 °C ( n = 4 mice per group). g IP of C/EBPα in isolated BM MKs from WT mice and Pnpla2 –/– mice under 30 °C or 4 °C. Acetyl-C/EBPα was detected. Non-immune IgG was used as a negative control. h Thrombocytopoiesis-associated gene expression in isolated MKs from WT mice and Pnpla2 –/– mice under 30 °C or 4 °C ( n = 3 samples per group). * P < 0.05; ** P < 0.01; *** P < 0.001. NS not significant. Data are presented as mean ± SD.

    Journal: Cell Research

    Article Title: Cold exposure aggravates vein occlusion through non-shivering thermogenesis-induced thrombocytopoiesis

    doi: 10.1038/s41422-026-01280-2

    Figure Lengend Snippet: a Diagram of lipolysis in an adipocyte in WT mice and Pnpla2 –/– mice. Pnpla2 encodes ATGL, a key intracellular lipase involved in the hydrolysis of stored fat and FFA release. Pnpla2 –/– mice are not able to liberate FFAs from adipose TG depots. b Weight quantification of BAT and WAT in WT mice and Pnpla2 –/– mice under 30 °C or 4 °C ( n = 4 samples per group). c Histological analysis of BAT and WAT in WT mice and Pnpla2 –/– mice under 30 °C or 4 °C. Quantification of adipocyte size ( n = 8 random fields per group). Scale bar: 100 μm. d Immunohistochemical staining of BAT and WAT with UCP1 and COX4, followed by counterstaining with DAPI (blue) in WT mice and Pnpla2 –/– mice under 30 °C or 4 °C. Quantification of UCP1 + signals and COX4 + signals ( n = 8 random fields per group). Scale bar: 50 μm. e c-FFA levels in WT mice and Pnpla2 –/– mice under 30 °C or 4 °C ( n = 4 mice per group). f PLT, PDW, and MPV analysis in PB from WT mice and Pnpla2 –/– mice under 30 °C or 4 °C ( n = 4 mice per group). g IP of C/EBPα in isolated BM MKs from WT mice and Pnpla2 –/– mice under 30 °C or 4 °C. Acetyl-C/EBPα was detected. Non-immune IgG was used as a negative control. h Thrombocytopoiesis-associated gene expression in isolated MKs from WT mice and Pnpla2 –/– mice under 30 °C or 4 °C ( n = 3 samples per group). * P < 0.05; ** P < 0.01; *** P < 0.001. NS not significant. Data are presented as mean ± SD.

    Article Snippet: For immunohistochemical staining of adipose tissues, paraffin-embedded tissue sections were stained with a rabbit anti-UCP1 antibody (1:100; Cat# A5857; ABclonal) or a rabbit anti-COX4 antibody (1:100; Cat# A6564; ABclonal).

    Techniques: Immunohistochemical staining, Staining, Isolation, Negative Control, Gene Expression

    (A) Relative mRNA expression of PGC-1a, NRF1, and TFAM in cellular Huntington’s disease models (Q23 and Q74). Gene expression was significantly reduced in HD conditions compared with control and was restored following Vitamin D supplementation. (B) Relative mitochondrial DNA (mtDNA) copy number determined by aPCR using mitochondrial genes normalized to nuclear genes in Q23 and Q74 cells. (C) Relative expression of the mitochondrial-encoded respiratory gene COX1 in Q23 and Q74 cellular models. HD conditions show decreased COXL expression, which is significantly increased upon Vitamin D treatment. (D) Relative protein expression of the nuclear-encoded mitochondrial respiratory subunit COX4 in cellular model of HD. (E) Proposed model illustrating the mechanism by which Vitamin D restores mitochondrial homeostasis in HD maodels. Bar plot is from three independent experiments (n = 3) and all values are presented as mean with SD; *p value calculated using unpaired Welch’s t-test with Holm’s correction *P < 0.05. *p <0.05, **p < 0.005, ***p <0.0005, and ****p < 0.00005).

    Journal: bioRxiv

    Article Title: The CYP27A1–VDR Feedback Rheostat Controls Mitochondrial Protein Homeostasis and Preserves Hippocampal-Striatal Network Integrity to rescue Cognitive impairment in HD condition

    doi: 10.64898/2026.06.11.731670

    Figure Lengend Snippet: (A) Relative mRNA expression of PGC-1a, NRF1, and TFAM in cellular Huntington’s disease models (Q23 and Q74). Gene expression was significantly reduced in HD conditions compared with control and was restored following Vitamin D supplementation. (B) Relative mitochondrial DNA (mtDNA) copy number determined by aPCR using mitochondrial genes normalized to nuclear genes in Q23 and Q74 cells. (C) Relative expression of the mitochondrial-encoded respiratory gene COX1 in Q23 and Q74 cellular models. HD conditions show decreased COXL expression, which is significantly increased upon Vitamin D treatment. (D) Relative protein expression of the nuclear-encoded mitochondrial respiratory subunit COX4 in cellular model of HD. (E) Proposed model illustrating the mechanism by which Vitamin D restores mitochondrial homeostasis in HD maodels. Bar plot is from three independent experiments (n = 3) and all values are presented as mean with SD; *p value calculated using unpaired Welch’s t-test with Holm’s correction *P < 0.05. *p <0.05, **p < 0.005, ***p <0.0005, and ****p < 0.00005).

    Article Snippet: The following antibodies were used: VDR (A23289, 1:1000, ABclonal), DRP1 (A21968, 1:1000, ABclonal), Mitofusin-1/MFN1 (A21293, 1:1000, ABclonal), Mitofusin-2/MFN2 (D2D10, 1:1000, CST), SDHB (A10821, 1:1000, ABclonal), β-Tubulin (AC008, 1:1000, ABclonal), FIS1 (E3K90, 1:1000, CST), SDHA (A13852, 1:1000, Abclonal), MFN1 (A21293, 1:1000, Abclonal), CHCHD4 (A25029, 1:1000, Abclonal), COX4 (A11631, 1:1000, Abclonal), TAFM (A3173, 1:1000, Abclonal).

    Techniques: Expressing, Gene Expression, Control