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rabbit polyclonal antibodies against pex16  (Proteintech)

 
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    Proteintech rabbit polyclonal antibodies against pex16
    (A) Gene expression analysis in BAT, iWAT, and gWAT of WT mice kept at normal room temperature (RT) (22°C) or subjected to cold (4°C) exposure; n = 3–4. (B) Fluorescence microscopy analysis of COS-7 cells transfected with a GFP reporter under the control of a –2 kb <t>Pex16</t> promoter alone or together with HA-PRDM16. Original magnification, ×20. (C) Luciferase reporter assay in COS-7 cells; n = 3. (D) BAT SVF cells expressing retrovirally encoded FLAG-PRDM16 were subjected to ChIP assay using an anti-FLAG antibody followed by qPCR using primers to amplify various regions of the Pex16 promoter; n = 6. *P < 0.05; **P < 0.01; ***P < 0.001. (E) Gene expression analysis in iWAT of control and adipose-specific PRDM16-KO (PRDM16-AKO) mice; n = 3. Data are expressed as mean ± SEM and were analyzed by Student’s t test. †P < 0.05 versus control RT; #P < 0.05 versus control cold.
    Rabbit Polyclonal Antibodies Against Pex16, supplied by Proteintech, 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/rabbit polyclonal antibodies against pex16/product/Proteintech
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit polyclonal antibodies against pex16 - by Bioz Stars, 2024-12
    93/100 stars

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    1) Product Images from "Peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission"

    Article Title: Peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI120606

    (A) Gene expression analysis in BAT, iWAT, and gWAT of WT mice kept at normal room temperature (RT) (22°C) or subjected to cold (4°C) exposure; n = 3–4. (B) Fluorescence microscopy analysis of COS-7 cells transfected with a GFP reporter under the control of a –2 kb Pex16 promoter alone or together with HA-PRDM16. Original magnification, ×20. (C) Luciferase reporter assay in COS-7 cells; n = 3. (D) BAT SVF cells expressing retrovirally encoded FLAG-PRDM16 were subjected to ChIP assay using an anti-FLAG antibody followed by qPCR using primers to amplify various regions of the Pex16 promoter; n = 6. *P < 0.05; **P < 0.01; ***P < 0.001. (E) Gene expression analysis in iWAT of control and adipose-specific PRDM16-KO (PRDM16-AKO) mice; n = 3. Data are expressed as mean ± SEM and were analyzed by Student’s t test. †P < 0.05 versus control RT; #P < 0.05 versus control cold.
    Figure Legend Snippet: (A) Gene expression analysis in BAT, iWAT, and gWAT of WT mice kept at normal room temperature (RT) (22°C) or subjected to cold (4°C) exposure; n = 3–4. (B) Fluorescence microscopy analysis of COS-7 cells transfected with a GFP reporter under the control of a –2 kb Pex16 promoter alone or together with HA-PRDM16. Original magnification, ×20. (C) Luciferase reporter assay in COS-7 cells; n = 3. (D) BAT SVF cells expressing retrovirally encoded FLAG-PRDM16 were subjected to ChIP assay using an anti-FLAG antibody followed by qPCR using primers to amplify various regions of the Pex16 promoter; n = 6. *P < 0.05; **P < 0.01; ***P < 0.001. (E) Gene expression analysis in iWAT of control and adipose-specific PRDM16-KO (PRDM16-AKO) mice; n = 3. Data are expressed as mean ± SEM and were analyzed by Student’s t test. †P < 0.05 versus control RT; #P < 0.05 versus control cold.

    Techniques Used: Expressing, Fluorescence, Microscopy, Transfection, Luciferase, Reporter Assay

    (A) Gene targeting strategy for Pex16 conditional knockout mice. (B) Analysis of Cre-mediated recombination by PCR. (C) Gene expression analysis; n = 3–6. (D) qPCR analysis demonstrating that Pex16 knockout does not affect gene expression of other peroxisomal genes in BAT; n = 5. (E) Immunofluorescence analysis using anti-PMP70–Atto 488 antibody in BAT of control and Pex16-AKO mice. Original magnification, ×60. (F) Western blot analysis in iWAT. Data in C and D are expressed as mean ± SEM and were analyzed by Student’s t test; ***P < 0.001.
    Figure Legend Snippet: (A) Gene targeting strategy for Pex16 conditional knockout mice. (B) Analysis of Cre-mediated recombination by PCR. (C) Gene expression analysis; n = 3–6. (D) qPCR analysis demonstrating that Pex16 knockout does not affect gene expression of other peroxisomal genes in BAT; n = 5. (E) Immunofluorescence analysis using anti-PMP70–Atto 488 antibody in BAT of control and Pex16-AKO mice. Original magnification, ×60. (F) Western blot analysis in iWAT. Data in C and D are expressed as mean ± SEM and were analyzed by Student’s t test; ***P < 0.001.

    Techniques Used: Knock-Out, Expressing, Immunofluorescence, Western Blot

    (A) Body weight of mice fed normal chow diet; n = 7–9. (B) Body weight of mice fed an HFD and maintained at 22°C; n = 9–11. (C) Body weight of mice fed an HFD and maintained at 30°C; n = 8. (D) MRI analysis of body composition in mice kept at room temperature after 20 weeks of high-fat feeding; n = 10. (E) Weight of gWAT from HFD-fed mice; n = 3. (F) H&E staining of gWAT from chow- and HFD-fed control and Pex16-AKO mice. The images are representative of 3 mice per genotype. (G) OCR (VO2) before and after intraperitoneal NE injection; n = 3–4. (H) H&E staining of BAT mice kept at room temperature or subjected to cold exposure. The images are representative of 3 mice per genotype. (I) Representative images (n = 3) of BAT from cold-treated mice. Original magnification, F and H, ×10. (J) Quantification of triglycerides (TG) in BAT; n = 3–4. (K) Rectal temperature of mice subjected to a 6-hour cold challenge; n = 7–9. (L) Kaplan-Meier survival curves of mice individually housed in InfraMot (TSE Systems) activity monitors stored at 4°C; n = 7–8. Data are expressed as mean ± SEM. Student’s t test was used for analysis of the data in B, D, E, and J. Two-way ANOVA with Bonferroni’s post hoc test was used for analysis of the data in G and K. To assess statistical significance in L, Mantel-Cox (log-rank) test was used. *P < 0.05; ***P < 0.001.
    Figure Legend Snippet: (A) Body weight of mice fed normal chow diet; n = 7–9. (B) Body weight of mice fed an HFD and maintained at 22°C; n = 9–11. (C) Body weight of mice fed an HFD and maintained at 30°C; n = 8. (D) MRI analysis of body composition in mice kept at room temperature after 20 weeks of high-fat feeding; n = 10. (E) Weight of gWAT from HFD-fed mice; n = 3. (F) H&E staining of gWAT from chow- and HFD-fed control and Pex16-AKO mice. The images are representative of 3 mice per genotype. (G) OCR (VO2) before and after intraperitoneal NE injection; n = 3–4. (H) H&E staining of BAT mice kept at room temperature or subjected to cold exposure. The images are representative of 3 mice per genotype. (I) Representative images (n = 3) of BAT from cold-treated mice. Original magnification, F and H, ×10. (J) Quantification of triglycerides (TG) in BAT; n = 3–4. (K) Rectal temperature of mice subjected to a 6-hour cold challenge; n = 7–9. (L) Kaplan-Meier survival curves of mice individually housed in InfraMot (TSE Systems) activity monitors stored at 4°C; n = 7–8. Data are expressed as mean ± SEM. Student’s t test was used for analysis of the data in B, D, E, and J. Two-way ANOVA with Bonferroni’s post hoc test was used for analysis of the data in G and K. To assess statistical significance in L, Mantel-Cox (log-rank) test was used. *P < 0.05; ***P < 0.001.

    Techniques Used: Staining, Injection, Activity Assay

    (A) TEM analysis of BAT from control and Pex16-AKO mice kept at room temperature or subjected to cold exposure. Peroxisomes (black dots) were detected by staining using DAB. Note the difference in mitochondrial morphology between the genotypes at 4°C. Scale bars: 500 nm. P, peroxisome; M, mitochondria; LD, lipid droplet. (B) Aspect ratio (ratio of major axis length to minor axis length) measured in BAT mitochondria. The data are based on 15 mitochondria per condition. (C) Number of mitochondria per cell based on TEM images of BAT taken at ×1000–×2000 magnification. Data are the average of 8 cells per condition. (D and E) mtDNA copy number normalized to nuclear DNA measured by qPCR in BAT and iWAT; for BAT, n = 6 per genotype at 22°C and 3 per genotype at 4°C; for iWAT, n = 4 per genotype under each condition. (F) Gene expression analysis in BAT of cold-treated mice; n = 4–5. Data are expressed as mean ± SEM and were analyzed by 1-way ANOVA followed by Fisher’s least significant difference (LSD) test (B–E) or by Student’s t test (F); *P < 0.05; **P < 0.01; ***P < 0.001.
    Figure Legend Snippet: (A) TEM analysis of BAT from control and Pex16-AKO mice kept at room temperature or subjected to cold exposure. Peroxisomes (black dots) were detected by staining using DAB. Note the difference in mitochondrial morphology between the genotypes at 4°C. Scale bars: 500 nm. P, peroxisome; M, mitochondria; LD, lipid droplet. (B) Aspect ratio (ratio of major axis length to minor axis length) measured in BAT mitochondria. The data are based on 15 mitochondria per condition. (C) Number of mitochondria per cell based on TEM images of BAT taken at ×1000–×2000 magnification. Data are the average of 8 cells per condition. (D and E) mtDNA copy number normalized to nuclear DNA measured by qPCR in BAT and iWAT; for BAT, n = 6 per genotype at 22°C and 3 per genotype at 4°C; for iWAT, n = 4 per genotype under each condition. (F) Gene expression analysis in BAT of cold-treated mice; n = 4–5. Data are expressed as mean ± SEM and were analyzed by 1-way ANOVA followed by Fisher’s least significant difference (LSD) test (B–E) or by Student’s t test (F); *P < 0.05; **P < 0.01; ***P < 0.001.

    Techniques Used: Staining, Expressing

    (A and B) BAT SVF cells were subjected to brown adipogenesis for 4 days and then treated with scrambled (SC) or Pex16 shRNA and analyzed after an additional 5 days using immunoblotting and mtDNA content measurement by qPCR. n = 3 in B. KD, knockdown. (C) BAT SVF cells stably expressing stably expressing Mito-roGFP were differentiated into adipocytes and then treated with scrambled or Pex16 shRNA in the presence or absence of Mdivi-1 and analyzed 5 days later for mitochondrial morphology using confocal microscopy. Images are representative of 3 separate experiments. Original magnification, ×60. (D) Quantification of mitochondrial morphology of the cells in C. (E) Effect of Pex16 knockdown on OCR measured in BAT SVF cells using a Seahorse XF24 Extracellular Flux Analyzer; n = 5. AA+R, mixture of antimycin A and rotenone. (F and G) Measurement of mitochondrial respiration using an OROBOROS Oxygraph system in permeabilized BAT and iWAT from control and Pex16-AKO mice following sequential additions of octanoyl-l-carnitine (OC); pyruvate (Pyr); glutamate and malate (G+M); adenosine diphosphate and succinate (ADP+S); and FCCP; n = 4–5. Data are expressed as mean ± SEM and were analyzed by Student’s t test; *P < 0.05; **P < 0.01.
    Figure Legend Snippet: (A and B) BAT SVF cells were subjected to brown adipogenesis for 4 days and then treated with scrambled (SC) or Pex16 shRNA and analyzed after an additional 5 days using immunoblotting and mtDNA content measurement by qPCR. n = 3 in B. KD, knockdown. (C) BAT SVF cells stably expressing stably expressing Mito-roGFP were differentiated into adipocytes and then treated with scrambled or Pex16 shRNA in the presence or absence of Mdivi-1 and analyzed 5 days later for mitochondrial morphology using confocal microscopy. Images are representative of 3 separate experiments. Original magnification, ×60. (D) Quantification of mitochondrial morphology of the cells in C. (E) Effect of Pex16 knockdown on OCR measured in BAT SVF cells using a Seahorse XF24 Extracellular Flux Analyzer; n = 5. AA+R, mixture of antimycin A and rotenone. (F and G) Measurement of mitochondrial respiration using an OROBOROS Oxygraph system in permeabilized BAT and iWAT from control and Pex16-AKO mice following sequential additions of octanoyl-l-carnitine (OC); pyruvate (Pyr); glutamate and malate (G+M); adenosine diphosphate and succinate (ADP+S); and FCCP; n = 4–5. Data are expressed as mean ± SEM and were analyzed by Student’s t test; *P < 0.05; **P < 0.01.

    Techniques Used: shRNA, Western Blot, Stable Transfection, Expressing, Confocal Microscopy

    (A) Analysis of Cre-mediated recombination by PCR. (B) Western blot analysis in BAT, iWAT, and gWAT. (C) Gene expression analysis by qPCR in BAT; n = 4–6. (D) OCR (VO2) measured in control and Pex16-BKO mice using indirect calorimetry before and after intraperitoneal NE injection; n = 4. (E) Rectal temperature of control and Pex16-BKO mice subjected to a 6-hour cold challenge; n = 5–6. (F) qPCR analysis in iWAT of mice subjected to an overnight cold exposure; n = 4–6. Data are expressed as mean ± SEM and were analyzed by Student’s t test (C and F) or 2-way ANOVA with Bonferroni’s post hoc test (D and E). *P < 0.05.
    Figure Legend Snippet: (A) Analysis of Cre-mediated recombination by PCR. (B) Western blot analysis in BAT, iWAT, and gWAT. (C) Gene expression analysis by qPCR in BAT; n = 4–6. (D) OCR (VO2) measured in control and Pex16-BKO mice using indirect calorimetry before and after intraperitoneal NE injection; n = 4. (E) Rectal temperature of control and Pex16-BKO mice subjected to a 6-hour cold challenge; n = 5–6. (F) qPCR analysis in iWAT of mice subjected to an overnight cold exposure; n = 4–6. Data are expressed as mean ± SEM and were analyzed by Student’s t test (C and F) or 2-way ANOVA with Bonferroni’s post hoc test (D and E). *P < 0.05.

    Techniques Used: Western Blot, Expressing, Injection

    (A) mRNA levels of FAO genes in BAT of control and Pex16-AKO mice; n = 3–13. (B and C) β-Oxidation of lignoceric acid (C24:0) and palmitic acid (C16:0) in BAT; n = 6–7. (D) Gene targeting strategy using CRISPR/Cas9 to insert loxP sites into the Acox1 locus. The floxed mice were crossed with an adiponectin-Cre mouse to generate Acox1-AKO mice. gRNA, guide RNA; ssODN, single-stranded oligodeoxyribonucleotide. (E) qPCR analysis of FAO and peroxisomal biogenesis genes; n = 3. (F) Western blot analysis of Acox1 knockout in BAT and iWAT. (G) Control and Acox1-KO iWAT SVF cells were incubated with D3-C22:0, whose catabolism to D3-C16:0 was measured mass spectrometrically. FAO was expressed as ratio of D3-C16:0 to D3-C22:0; n = 4. (H) Body weight of control and Acox1-AKO mice fed an HFD and maintained at normal room temperature; n = 13–18. (I) Cold tolerance was determined by measuring rectal temperature at the indicated times after cold exposure; n = 4–5. (J) mtDNA content normalized to nuclear DNA in BAT of control and Acox1-AKO mice subjected to cold exposure; n = 3. Data are expressed as mean ± SEM. Student’s t test was used for analysis of the data in A–C, E, G, and J were analyzed by Student’s t test. Two-way ANOVA with Bonferroni’s post hoc test was used for analysis of the data in I. *P < 0.05; **P < 0.01; ***P < 0.001.
    Figure Legend Snippet: (A) mRNA levels of FAO genes in BAT of control and Pex16-AKO mice; n = 3–13. (B and C) β-Oxidation of lignoceric acid (C24:0) and palmitic acid (C16:0) in BAT; n = 6–7. (D) Gene targeting strategy using CRISPR/Cas9 to insert loxP sites into the Acox1 locus. The floxed mice were crossed with an adiponectin-Cre mouse to generate Acox1-AKO mice. gRNA, guide RNA; ssODN, single-stranded oligodeoxyribonucleotide. (E) qPCR analysis of FAO and peroxisomal biogenesis genes; n = 3. (F) Western blot analysis of Acox1 knockout in BAT and iWAT. (G) Control and Acox1-KO iWAT SVF cells were incubated with D3-C22:0, whose catabolism to D3-C16:0 was measured mass spectrometrically. FAO was expressed as ratio of D3-C16:0 to D3-C22:0; n = 4. (H) Body weight of control and Acox1-AKO mice fed an HFD and maintained at normal room temperature; n = 13–18. (I) Cold tolerance was determined by measuring rectal temperature at the indicated times after cold exposure; n = 4–5. (J) mtDNA content normalized to nuclear DNA in BAT of control and Acox1-AKO mice subjected to cold exposure; n = 3. Data are expressed as mean ± SEM. Student’s t test was used for analysis of the data in A–C, E, G, and J were analyzed by Student’s t test. Two-way ANOVA with Bonferroni’s post hoc test was used for analysis of the data in I. *P < 0.05; **P < 0.01; ***P < 0.001.

    Techniques Used: CRISPR, Western Blot, Knock-Out, Incubation

    (A) Ether lipid synthetic pathway. The initial steps for synthesis of ether lipids, including plasmalogens, take place in peroxisomes, generating 1-O-alkyl-glycerol-3-phosphate (AGP), a precursor for ether-linked analogs of PC and phosphatidylethanolamine. DHAP, dihydroxyacetone phosphate. (B and C) Western blot analysis suggesting that ether lipid synthetic enzymes are degraded in BAT (B) and iWAT (C) of Pex16-AKO mice (D) Targeted lipidomics analysis of mitochondrial phospholipids in BAT of WT C57 mice. PS, phosphatidylserine; PG, phosphatidylglycerol; aPC, alkyl ether PC; pPC, plasmalogen PC; PE, phosphatidylethanolamine; pPE, plasmalogen PE; n = 5. (E) Levels of various plasmalogen PE species in the mitochondrial fraction of BAT; n = 9–10. (F) Total diacyl and plasmalogen PE content in BAT mitochondria. (G) BAT SVF cells stably expressing Mito-roGFP were differentiated into adipocytes and then treated with scrambled or GNPAT shRNA and analyzed 5 days later for mitochondrial morphology using confocal microscopy. Images are representative of 3 separate experiments. Original magnification, ×60. (H) Differentiated BAT SVF cells were treated with scrambled or GNPAT shRNA. Five days later, mtDNA copy number normalized to nuclear DNA was measured by qPCR; n = 5. (I) Effect of shRNA-mediated knockdown of GNPAT on OCR was measured in BAT SVF cells using a Seahorse XF24 Extracellular Flux Analyzer; n = 8. Data are expressed as mean ± SEM and were analyzed by Student’s t test. *P < 0.05.
    Figure Legend Snippet: (A) Ether lipid synthetic pathway. The initial steps for synthesis of ether lipids, including plasmalogens, take place in peroxisomes, generating 1-O-alkyl-glycerol-3-phosphate (AGP), a precursor for ether-linked analogs of PC and phosphatidylethanolamine. DHAP, dihydroxyacetone phosphate. (B and C) Western blot analysis suggesting that ether lipid synthetic enzymes are degraded in BAT (B) and iWAT (C) of Pex16-AKO mice (D) Targeted lipidomics analysis of mitochondrial phospholipids in BAT of WT C57 mice. PS, phosphatidylserine; PG, phosphatidylglycerol; aPC, alkyl ether PC; pPC, plasmalogen PC; PE, phosphatidylethanolamine; pPE, plasmalogen PE; n = 5. (E) Levels of various plasmalogen PE species in the mitochondrial fraction of BAT; n = 9–10. (F) Total diacyl and plasmalogen PE content in BAT mitochondria. (G) BAT SVF cells stably expressing Mito-roGFP were differentiated into adipocytes and then treated with scrambled or GNPAT shRNA and analyzed 5 days later for mitochondrial morphology using confocal microscopy. Images are representative of 3 separate experiments. Original magnification, ×60. (H) Differentiated BAT SVF cells were treated with scrambled or GNPAT shRNA. Five days later, mtDNA copy number normalized to nuclear DNA was measured by qPCR; n = 5. (I) Effect of shRNA-mediated knockdown of GNPAT on OCR was measured in BAT SVF cells using a Seahorse XF24 Extracellular Flux Analyzer; n = 8. Data are expressed as mean ± SEM and were analyzed by Student’s t test. *P < 0.05.

    Techniques Used: Western Blot, Stable Transfection, Expressing, shRNA, Confocal Microscopy

    (A) Mass spectrometric analysis of PE plasmalogens in the mitochondrial fractions from control and Pex16-AKO mice treated with or without AG for 8 weeks; n = 5. (B) TEM analysis of mitochondrial morphology in BAT of control and Pex16-AKO treated with or without AG, followed by cold exposure. Scale bar: 500 nm. (C) Aspect ratio measured in BAT mitochondria from control and Pex16-AKO mice. The data are based on 26 mitochondria per condition. (D) Number of mitochondria per cell based on TEM images of BAT taken at ×1000–×2000 magnification. The data are average of 6–8 cells per condition. (E) mtDNA measured by PCR in BAT of control and Pex16-AKO mice treated with or without AG, followed by cold exposure; n = 6–7. (F) VO2 was measured using indirect calorimetry before and after intraperitoneal NE injection; n = 8–9. (G). Cold tolerance was determined by measuring rectal temperature prior to and after 6 hours of cold exposure; n = 6–8. (H and I) Fatty acid and pyruvate oxidation assays in BAT; n = 3–4. Data are expressed as mean ± SEM and were analyzed by 1-way ANOVA, followed by Fisher’s LSD test (A, C–E, and G–I), or 2-way ANOVA with Bonferroni’s post hoc test (F); *P < 0.05; **P < 0.01; ***P < 0.001.
    Figure Legend Snippet: (A) Mass spectrometric analysis of PE plasmalogens in the mitochondrial fractions from control and Pex16-AKO mice treated with or without AG for 8 weeks; n = 5. (B) TEM analysis of mitochondrial morphology in BAT of control and Pex16-AKO treated with or without AG, followed by cold exposure. Scale bar: 500 nm. (C) Aspect ratio measured in BAT mitochondria from control and Pex16-AKO mice. The data are based on 26 mitochondria per condition. (D) Number of mitochondria per cell based on TEM images of BAT taken at ×1000–×2000 magnification. The data are average of 6–8 cells per condition. (E) mtDNA measured by PCR in BAT of control and Pex16-AKO mice treated with or without AG, followed by cold exposure; n = 6–7. (F) VO2 was measured using indirect calorimetry before and after intraperitoneal NE injection; n = 8–9. (G). Cold tolerance was determined by measuring rectal temperature prior to and after 6 hours of cold exposure; n = 6–8. (H and I) Fatty acid and pyruvate oxidation assays in BAT; n = 3–4. Data are expressed as mean ± SEM and were analyzed by 1-way ANOVA, followed by Fisher’s LSD test (A, C–E, and G–I), or 2-way ANOVA with Bonferroni’s post hoc test (F); *P < 0.05; **P < 0.01; ***P < 0.001.

    Techniques Used: Injection



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    rabbit polyclonal antibodies against pex16  (Proteintech)
    93
    Proteintech rabbit polyclonal antibodies against pex16
    (A) Gene expression analysis in BAT, iWAT, and gWAT of WT mice kept at normal room temperature (RT) (22°C) or subjected to cold (4°C) exposure; n = 3–4. (B) Fluorescence microscopy analysis of COS-7 cells transfected with a GFP reporter under the control of a –2 kb <t>Pex16</t> promoter alone or together with HA-PRDM16. Original magnification, ×20. (C) Luciferase reporter assay in COS-7 cells; n = 3. (D) BAT SVF cells expressing retrovirally encoded FLAG-PRDM16 were subjected to ChIP assay using an anti-FLAG antibody followed by qPCR using primers to amplify various regions of the Pex16 promoter; n = 6. *P < 0.05; **P < 0.01; ***P < 0.001. (E) Gene expression analysis in iWAT of control and adipose-specific PRDM16-KO (PRDM16-AKO) mice; n = 3. Data are expressed as mean ± SEM and were analyzed by Student’s t test. †P < 0.05 versus control RT; #P < 0.05 versus control cold.
    Rabbit Polyclonal Antibodies Against Pex16, supplied by Proteintech, 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/rabbit polyclonal antibodies against pex16/product/Proteintech
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit polyclonal antibodies against pex16 - by Bioz Stars, 2024-12
    93/100 stars
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    Image Search Results


    (A) Gene expression analysis in BAT, iWAT, and gWAT of WT mice kept at normal room temperature (RT) (22°C) or subjected to cold (4°C) exposure; n = 3–4. (B) Fluorescence microscopy analysis of COS-7 cells transfected with a GFP reporter under the control of a –2 kb Pex16 promoter alone or together with HA-PRDM16. Original magnification, ×20. (C) Luciferase reporter assay in COS-7 cells; n = 3. (D) BAT SVF cells expressing retrovirally encoded FLAG-PRDM16 were subjected to ChIP assay using an anti-FLAG antibody followed by qPCR using primers to amplify various regions of the Pex16 promoter; n = 6. *P < 0.05; **P < 0.01; ***P < 0.001. (E) Gene expression analysis in iWAT of control and adipose-specific PRDM16-KO (PRDM16-AKO) mice; n = 3. Data are expressed as mean ± SEM and were analyzed by Student’s t test. †P < 0.05 versus control RT; #P < 0.05 versus control cold.

    Journal: The Journal of Clinical Investigation

    Article Title: Peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission

    doi: 10.1172/JCI120606

    Figure Lengend Snippet: (A) Gene expression analysis in BAT, iWAT, and gWAT of WT mice kept at normal room temperature (RT) (22°C) or subjected to cold (4°C) exposure; n = 3–4. (B) Fluorescence microscopy analysis of COS-7 cells transfected with a GFP reporter under the control of a –2 kb Pex16 promoter alone or together with HA-PRDM16. Original magnification, ×20. (C) Luciferase reporter assay in COS-7 cells; n = 3. (D) BAT SVF cells expressing retrovirally encoded FLAG-PRDM16 were subjected to ChIP assay using an anti-FLAG antibody followed by qPCR using primers to amplify various regions of the Pex16 promoter; n = 6. *P < 0.05; **P < 0.01; ***P < 0.001. (E) Gene expression analysis in iWAT of control and adipose-specific PRDM16-KO (PRDM16-AKO) mice; n = 3. Data are expressed as mean ± SEM and were analyzed by Student’s t test. †P < 0.05 versus control RT; #P < 0.05 versus control cold.

    Article Snippet: Rabbit polyclonal antibodies against Pex16 (1:1000; catalog 14816-1-AP), Acox1 (1:1000; catalog 10957-1-AP), and GNPAT (1:1000; catalog 14931-1-AP) were from Proteintech.

    Techniques: Expressing, Fluorescence, Microscopy, Transfection, Luciferase, Reporter Assay

    (A) Gene targeting strategy for Pex16 conditional knockout mice. (B) Analysis of Cre-mediated recombination by PCR. (C) Gene expression analysis; n = 3–6. (D) qPCR analysis demonstrating that Pex16 knockout does not affect gene expression of other peroxisomal genes in BAT; n = 5. (E) Immunofluorescence analysis using anti-PMP70–Atto 488 antibody in BAT of control and Pex16-AKO mice. Original magnification, ×60. (F) Western blot analysis in iWAT. Data in C and D are expressed as mean ± SEM and were analyzed by Student’s t test; ***P < 0.001.

    Journal: The Journal of Clinical Investigation

    Article Title: Peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission

    doi: 10.1172/JCI120606

    Figure Lengend Snippet: (A) Gene targeting strategy for Pex16 conditional knockout mice. (B) Analysis of Cre-mediated recombination by PCR. (C) Gene expression analysis; n = 3–6. (D) qPCR analysis demonstrating that Pex16 knockout does not affect gene expression of other peroxisomal genes in BAT; n = 5. (E) Immunofluorescence analysis using anti-PMP70–Atto 488 antibody in BAT of control and Pex16-AKO mice. Original magnification, ×60. (F) Western blot analysis in iWAT. Data in C and D are expressed as mean ± SEM and were analyzed by Student’s t test; ***P < 0.001.

    Article Snippet: Rabbit polyclonal antibodies against Pex16 (1:1000; catalog 14816-1-AP), Acox1 (1:1000; catalog 10957-1-AP), and GNPAT (1:1000; catalog 14931-1-AP) were from Proteintech.

    Techniques: Knock-Out, Expressing, Immunofluorescence, Western Blot

    (A) Body weight of mice fed normal chow diet; n = 7–9. (B) Body weight of mice fed an HFD and maintained at 22°C; n = 9–11. (C) Body weight of mice fed an HFD and maintained at 30°C; n = 8. (D) MRI analysis of body composition in mice kept at room temperature after 20 weeks of high-fat feeding; n = 10. (E) Weight of gWAT from HFD-fed mice; n = 3. (F) H&E staining of gWAT from chow- and HFD-fed control and Pex16-AKO mice. The images are representative of 3 mice per genotype. (G) OCR (VO2) before and after intraperitoneal NE injection; n = 3–4. (H) H&E staining of BAT mice kept at room temperature or subjected to cold exposure. The images are representative of 3 mice per genotype. (I) Representative images (n = 3) of BAT from cold-treated mice. Original magnification, F and H, ×10. (J) Quantification of triglycerides (TG) in BAT; n = 3–4. (K) Rectal temperature of mice subjected to a 6-hour cold challenge; n = 7–9. (L) Kaplan-Meier survival curves of mice individually housed in InfraMot (TSE Systems) activity monitors stored at 4°C; n = 7–8. Data are expressed as mean ± SEM. Student’s t test was used for analysis of the data in B, D, E, and J. Two-way ANOVA with Bonferroni’s post hoc test was used for analysis of the data in G and K. To assess statistical significance in L, Mantel-Cox (log-rank) test was used. *P < 0.05; ***P < 0.001.

    Journal: The Journal of Clinical Investigation

    Article Title: Peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission

    doi: 10.1172/JCI120606

    Figure Lengend Snippet: (A) Body weight of mice fed normal chow diet; n = 7–9. (B) Body weight of mice fed an HFD and maintained at 22°C; n = 9–11. (C) Body weight of mice fed an HFD and maintained at 30°C; n = 8. (D) MRI analysis of body composition in mice kept at room temperature after 20 weeks of high-fat feeding; n = 10. (E) Weight of gWAT from HFD-fed mice; n = 3. (F) H&E staining of gWAT from chow- and HFD-fed control and Pex16-AKO mice. The images are representative of 3 mice per genotype. (G) OCR (VO2) before and after intraperitoneal NE injection; n = 3–4. (H) H&E staining of BAT mice kept at room temperature or subjected to cold exposure. The images are representative of 3 mice per genotype. (I) Representative images (n = 3) of BAT from cold-treated mice. Original magnification, F and H, ×10. (J) Quantification of triglycerides (TG) in BAT; n = 3–4. (K) Rectal temperature of mice subjected to a 6-hour cold challenge; n = 7–9. (L) Kaplan-Meier survival curves of mice individually housed in InfraMot (TSE Systems) activity monitors stored at 4°C; n = 7–8. Data are expressed as mean ± SEM. Student’s t test was used for analysis of the data in B, D, E, and J. Two-way ANOVA with Bonferroni’s post hoc test was used for analysis of the data in G and K. To assess statistical significance in L, Mantel-Cox (log-rank) test was used. *P < 0.05; ***P < 0.001.

    Article Snippet: Rabbit polyclonal antibodies against Pex16 (1:1000; catalog 14816-1-AP), Acox1 (1:1000; catalog 10957-1-AP), and GNPAT (1:1000; catalog 14931-1-AP) were from Proteintech.

    Techniques: Staining, Injection, Activity Assay

    (A) TEM analysis of BAT from control and Pex16-AKO mice kept at room temperature or subjected to cold exposure. Peroxisomes (black dots) were detected by staining using DAB. Note the difference in mitochondrial morphology between the genotypes at 4°C. Scale bars: 500 nm. P, peroxisome; M, mitochondria; LD, lipid droplet. (B) Aspect ratio (ratio of major axis length to minor axis length) measured in BAT mitochondria. The data are based on 15 mitochondria per condition. (C) Number of mitochondria per cell based on TEM images of BAT taken at ×1000–×2000 magnification. Data are the average of 8 cells per condition. (D and E) mtDNA copy number normalized to nuclear DNA measured by qPCR in BAT and iWAT; for BAT, n = 6 per genotype at 22°C and 3 per genotype at 4°C; for iWAT, n = 4 per genotype under each condition. (F) Gene expression analysis in BAT of cold-treated mice; n = 4–5. Data are expressed as mean ± SEM and were analyzed by 1-way ANOVA followed by Fisher’s least significant difference (LSD) test (B–E) or by Student’s t test (F); *P < 0.05; **P < 0.01; ***P < 0.001.

    Journal: The Journal of Clinical Investigation

    Article Title: Peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission

    doi: 10.1172/JCI120606

    Figure Lengend Snippet: (A) TEM analysis of BAT from control and Pex16-AKO mice kept at room temperature or subjected to cold exposure. Peroxisomes (black dots) were detected by staining using DAB. Note the difference in mitochondrial morphology between the genotypes at 4°C. Scale bars: 500 nm. P, peroxisome; M, mitochondria; LD, lipid droplet. (B) Aspect ratio (ratio of major axis length to minor axis length) measured in BAT mitochondria. The data are based on 15 mitochondria per condition. (C) Number of mitochondria per cell based on TEM images of BAT taken at ×1000–×2000 magnification. Data are the average of 8 cells per condition. (D and E) mtDNA copy number normalized to nuclear DNA measured by qPCR in BAT and iWAT; for BAT, n = 6 per genotype at 22°C and 3 per genotype at 4°C; for iWAT, n = 4 per genotype under each condition. (F) Gene expression analysis in BAT of cold-treated mice; n = 4–5. Data are expressed as mean ± SEM and were analyzed by 1-way ANOVA followed by Fisher’s least significant difference (LSD) test (B–E) or by Student’s t test (F); *P < 0.05; **P < 0.01; ***P < 0.001.

    Article Snippet: Rabbit polyclonal antibodies against Pex16 (1:1000; catalog 14816-1-AP), Acox1 (1:1000; catalog 10957-1-AP), and GNPAT (1:1000; catalog 14931-1-AP) were from Proteintech.

    Techniques: Staining, Expressing

    (A and B) BAT SVF cells were subjected to brown adipogenesis for 4 days and then treated with scrambled (SC) or Pex16 shRNA and analyzed after an additional 5 days using immunoblotting and mtDNA content measurement by qPCR. n = 3 in B. KD, knockdown. (C) BAT SVF cells stably expressing stably expressing Mito-roGFP were differentiated into adipocytes and then treated with scrambled or Pex16 shRNA in the presence or absence of Mdivi-1 and analyzed 5 days later for mitochondrial morphology using confocal microscopy. Images are representative of 3 separate experiments. Original magnification, ×60. (D) Quantification of mitochondrial morphology of the cells in C. (E) Effect of Pex16 knockdown on OCR measured in BAT SVF cells using a Seahorse XF24 Extracellular Flux Analyzer; n = 5. AA+R, mixture of antimycin A and rotenone. (F and G) Measurement of mitochondrial respiration using an OROBOROS Oxygraph system in permeabilized BAT and iWAT from control and Pex16-AKO mice following sequential additions of octanoyl-l-carnitine (OC); pyruvate (Pyr); glutamate and malate (G+M); adenosine diphosphate and succinate (ADP+S); and FCCP; n = 4–5. Data are expressed as mean ± SEM and were analyzed by Student’s t test; *P < 0.05; **P < 0.01.

    Journal: The Journal of Clinical Investigation

    Article Title: Peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission

    doi: 10.1172/JCI120606

    Figure Lengend Snippet: (A and B) BAT SVF cells were subjected to brown adipogenesis for 4 days and then treated with scrambled (SC) or Pex16 shRNA and analyzed after an additional 5 days using immunoblotting and mtDNA content measurement by qPCR. n = 3 in B. KD, knockdown. (C) BAT SVF cells stably expressing stably expressing Mito-roGFP were differentiated into adipocytes and then treated with scrambled or Pex16 shRNA in the presence or absence of Mdivi-1 and analyzed 5 days later for mitochondrial morphology using confocal microscopy. Images are representative of 3 separate experiments. Original magnification, ×60. (D) Quantification of mitochondrial morphology of the cells in C. (E) Effect of Pex16 knockdown on OCR measured in BAT SVF cells using a Seahorse XF24 Extracellular Flux Analyzer; n = 5. AA+R, mixture of antimycin A and rotenone. (F and G) Measurement of mitochondrial respiration using an OROBOROS Oxygraph system in permeabilized BAT and iWAT from control and Pex16-AKO mice following sequential additions of octanoyl-l-carnitine (OC); pyruvate (Pyr); glutamate and malate (G+M); adenosine diphosphate and succinate (ADP+S); and FCCP; n = 4–5. Data are expressed as mean ± SEM and were analyzed by Student’s t test; *P < 0.05; **P < 0.01.

    Article Snippet: Rabbit polyclonal antibodies against Pex16 (1:1000; catalog 14816-1-AP), Acox1 (1:1000; catalog 10957-1-AP), and GNPAT (1:1000; catalog 14931-1-AP) were from Proteintech.

    Techniques: shRNA, Western Blot, Stable Transfection, Expressing, Confocal Microscopy

    (A) Analysis of Cre-mediated recombination by PCR. (B) Western blot analysis in BAT, iWAT, and gWAT. (C) Gene expression analysis by qPCR in BAT; n = 4–6. (D) OCR (VO2) measured in control and Pex16-BKO mice using indirect calorimetry before and after intraperitoneal NE injection; n = 4. (E) Rectal temperature of control and Pex16-BKO mice subjected to a 6-hour cold challenge; n = 5–6. (F) qPCR analysis in iWAT of mice subjected to an overnight cold exposure; n = 4–6. Data are expressed as mean ± SEM and were analyzed by Student’s t test (C and F) or 2-way ANOVA with Bonferroni’s post hoc test (D and E). *P < 0.05.

    Journal: The Journal of Clinical Investigation

    Article Title: Peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission

    doi: 10.1172/JCI120606

    Figure Lengend Snippet: (A) Analysis of Cre-mediated recombination by PCR. (B) Western blot analysis in BAT, iWAT, and gWAT. (C) Gene expression analysis by qPCR in BAT; n = 4–6. (D) OCR (VO2) measured in control and Pex16-BKO mice using indirect calorimetry before and after intraperitoneal NE injection; n = 4. (E) Rectal temperature of control and Pex16-BKO mice subjected to a 6-hour cold challenge; n = 5–6. (F) qPCR analysis in iWAT of mice subjected to an overnight cold exposure; n = 4–6. Data are expressed as mean ± SEM and were analyzed by Student’s t test (C and F) or 2-way ANOVA with Bonferroni’s post hoc test (D and E). *P < 0.05.

    Article Snippet: Rabbit polyclonal antibodies against Pex16 (1:1000; catalog 14816-1-AP), Acox1 (1:1000; catalog 10957-1-AP), and GNPAT (1:1000; catalog 14931-1-AP) were from Proteintech.

    Techniques: Western Blot, Expressing, Injection

    (A) mRNA levels of FAO genes in BAT of control and Pex16-AKO mice; n = 3–13. (B and C) β-Oxidation of lignoceric acid (C24:0) and palmitic acid (C16:0) in BAT; n = 6–7. (D) Gene targeting strategy using CRISPR/Cas9 to insert loxP sites into the Acox1 locus. The floxed mice were crossed with an adiponectin-Cre mouse to generate Acox1-AKO mice. gRNA, guide RNA; ssODN, single-stranded oligodeoxyribonucleotide. (E) qPCR analysis of FAO and peroxisomal biogenesis genes; n = 3. (F) Western blot analysis of Acox1 knockout in BAT and iWAT. (G) Control and Acox1-KO iWAT SVF cells were incubated with D3-C22:0, whose catabolism to D3-C16:0 was measured mass spectrometrically. FAO was expressed as ratio of D3-C16:0 to D3-C22:0; n = 4. (H) Body weight of control and Acox1-AKO mice fed an HFD and maintained at normal room temperature; n = 13–18. (I) Cold tolerance was determined by measuring rectal temperature at the indicated times after cold exposure; n = 4–5. (J) mtDNA content normalized to nuclear DNA in BAT of control and Acox1-AKO mice subjected to cold exposure; n = 3. Data are expressed as mean ± SEM. Student’s t test was used for analysis of the data in A–C, E, G, and J were analyzed by Student’s t test. Two-way ANOVA with Bonferroni’s post hoc test was used for analysis of the data in I. *P < 0.05; **P < 0.01; ***P < 0.001.

    Journal: The Journal of Clinical Investigation

    Article Title: Peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission

    doi: 10.1172/JCI120606

    Figure Lengend Snippet: (A) mRNA levels of FAO genes in BAT of control and Pex16-AKO mice; n = 3–13. (B and C) β-Oxidation of lignoceric acid (C24:0) and palmitic acid (C16:0) in BAT; n = 6–7. (D) Gene targeting strategy using CRISPR/Cas9 to insert loxP sites into the Acox1 locus. The floxed mice were crossed with an adiponectin-Cre mouse to generate Acox1-AKO mice. gRNA, guide RNA; ssODN, single-stranded oligodeoxyribonucleotide. (E) qPCR analysis of FAO and peroxisomal biogenesis genes; n = 3. (F) Western blot analysis of Acox1 knockout in BAT and iWAT. (G) Control and Acox1-KO iWAT SVF cells were incubated with D3-C22:0, whose catabolism to D3-C16:0 was measured mass spectrometrically. FAO was expressed as ratio of D3-C16:0 to D3-C22:0; n = 4. (H) Body weight of control and Acox1-AKO mice fed an HFD and maintained at normal room temperature; n = 13–18. (I) Cold tolerance was determined by measuring rectal temperature at the indicated times after cold exposure; n = 4–5. (J) mtDNA content normalized to nuclear DNA in BAT of control and Acox1-AKO mice subjected to cold exposure; n = 3. Data are expressed as mean ± SEM. Student’s t test was used for analysis of the data in A–C, E, G, and J were analyzed by Student’s t test. Two-way ANOVA with Bonferroni’s post hoc test was used for analysis of the data in I. *P < 0.05; **P < 0.01; ***P < 0.001.

    Article Snippet: Rabbit polyclonal antibodies against Pex16 (1:1000; catalog 14816-1-AP), Acox1 (1:1000; catalog 10957-1-AP), and GNPAT (1:1000; catalog 14931-1-AP) were from Proteintech.

    Techniques: CRISPR, Western Blot, Knock-Out, Incubation

    (A) Ether lipid synthetic pathway. The initial steps for synthesis of ether lipids, including plasmalogens, take place in peroxisomes, generating 1-O-alkyl-glycerol-3-phosphate (AGP), a precursor for ether-linked analogs of PC and phosphatidylethanolamine. DHAP, dihydroxyacetone phosphate. (B and C) Western blot analysis suggesting that ether lipid synthetic enzymes are degraded in BAT (B) and iWAT (C) of Pex16-AKO mice (D) Targeted lipidomics analysis of mitochondrial phospholipids in BAT of WT C57 mice. PS, phosphatidylserine; PG, phosphatidylglycerol; aPC, alkyl ether PC; pPC, plasmalogen PC; PE, phosphatidylethanolamine; pPE, plasmalogen PE; n = 5. (E) Levels of various plasmalogen PE species in the mitochondrial fraction of BAT; n = 9–10. (F) Total diacyl and plasmalogen PE content in BAT mitochondria. (G) BAT SVF cells stably expressing Mito-roGFP were differentiated into adipocytes and then treated with scrambled or GNPAT shRNA and analyzed 5 days later for mitochondrial morphology using confocal microscopy. Images are representative of 3 separate experiments. Original magnification, ×60. (H) Differentiated BAT SVF cells were treated with scrambled or GNPAT shRNA. Five days later, mtDNA copy number normalized to nuclear DNA was measured by qPCR; n = 5. (I) Effect of shRNA-mediated knockdown of GNPAT on OCR was measured in BAT SVF cells using a Seahorse XF24 Extracellular Flux Analyzer; n = 8. Data are expressed as mean ± SEM and were analyzed by Student’s t test. *P < 0.05.

    Journal: The Journal of Clinical Investigation

    Article Title: Peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission

    doi: 10.1172/JCI120606

    Figure Lengend Snippet: (A) Ether lipid synthetic pathway. The initial steps for synthesis of ether lipids, including plasmalogens, take place in peroxisomes, generating 1-O-alkyl-glycerol-3-phosphate (AGP), a precursor for ether-linked analogs of PC and phosphatidylethanolamine. DHAP, dihydroxyacetone phosphate. (B and C) Western blot analysis suggesting that ether lipid synthetic enzymes are degraded in BAT (B) and iWAT (C) of Pex16-AKO mice (D) Targeted lipidomics analysis of mitochondrial phospholipids in BAT of WT C57 mice. PS, phosphatidylserine; PG, phosphatidylglycerol; aPC, alkyl ether PC; pPC, plasmalogen PC; PE, phosphatidylethanolamine; pPE, plasmalogen PE; n = 5. (E) Levels of various plasmalogen PE species in the mitochondrial fraction of BAT; n = 9–10. (F) Total diacyl and plasmalogen PE content in BAT mitochondria. (G) BAT SVF cells stably expressing Mito-roGFP were differentiated into adipocytes and then treated with scrambled or GNPAT shRNA and analyzed 5 days later for mitochondrial morphology using confocal microscopy. Images are representative of 3 separate experiments. Original magnification, ×60. (H) Differentiated BAT SVF cells were treated with scrambled or GNPAT shRNA. Five days later, mtDNA copy number normalized to nuclear DNA was measured by qPCR; n = 5. (I) Effect of shRNA-mediated knockdown of GNPAT on OCR was measured in BAT SVF cells using a Seahorse XF24 Extracellular Flux Analyzer; n = 8. Data are expressed as mean ± SEM and were analyzed by Student’s t test. *P < 0.05.

    Article Snippet: Rabbit polyclonal antibodies against Pex16 (1:1000; catalog 14816-1-AP), Acox1 (1:1000; catalog 10957-1-AP), and GNPAT (1:1000; catalog 14931-1-AP) were from Proteintech.

    Techniques: Western Blot, Stable Transfection, Expressing, shRNA, Confocal Microscopy

    (A) Mass spectrometric analysis of PE plasmalogens in the mitochondrial fractions from control and Pex16-AKO mice treated with or without AG for 8 weeks; n = 5. (B) TEM analysis of mitochondrial morphology in BAT of control and Pex16-AKO treated with or without AG, followed by cold exposure. Scale bar: 500 nm. (C) Aspect ratio measured in BAT mitochondria from control and Pex16-AKO mice. The data are based on 26 mitochondria per condition. (D) Number of mitochondria per cell based on TEM images of BAT taken at ×1000–×2000 magnification. The data are average of 6–8 cells per condition. (E) mtDNA measured by PCR in BAT of control and Pex16-AKO mice treated with or without AG, followed by cold exposure; n = 6–7. (F) VO2 was measured using indirect calorimetry before and after intraperitoneal NE injection; n = 8–9. (G). Cold tolerance was determined by measuring rectal temperature prior to and after 6 hours of cold exposure; n = 6–8. (H and I) Fatty acid and pyruvate oxidation assays in BAT; n = 3–4. Data are expressed as mean ± SEM and were analyzed by 1-way ANOVA, followed by Fisher’s LSD test (A, C–E, and G–I), or 2-way ANOVA with Bonferroni’s post hoc test (F); *P < 0.05; **P < 0.01; ***P < 0.001.

    Journal: The Journal of Clinical Investigation

    Article Title: Peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission

    doi: 10.1172/JCI120606

    Figure Lengend Snippet: (A) Mass spectrometric analysis of PE plasmalogens in the mitochondrial fractions from control and Pex16-AKO mice treated with or without AG for 8 weeks; n = 5. (B) TEM analysis of mitochondrial morphology in BAT of control and Pex16-AKO treated with or without AG, followed by cold exposure. Scale bar: 500 nm. (C) Aspect ratio measured in BAT mitochondria from control and Pex16-AKO mice. The data are based on 26 mitochondria per condition. (D) Number of mitochondria per cell based on TEM images of BAT taken at ×1000–×2000 magnification. The data are average of 6–8 cells per condition. (E) mtDNA measured by PCR in BAT of control and Pex16-AKO mice treated with or without AG, followed by cold exposure; n = 6–7. (F) VO2 was measured using indirect calorimetry before and after intraperitoneal NE injection; n = 8–9. (G). Cold tolerance was determined by measuring rectal temperature prior to and after 6 hours of cold exposure; n = 6–8. (H and I) Fatty acid and pyruvate oxidation assays in BAT; n = 3–4. Data are expressed as mean ± SEM and were analyzed by 1-way ANOVA, followed by Fisher’s LSD test (A, C–E, and G–I), or 2-way ANOVA with Bonferroni’s post hoc test (F); *P < 0.05; **P < 0.01; ***P < 0.001.

    Article Snippet: Rabbit polyclonal antibodies against Pex16 (1:1000; catalog 14816-1-AP), Acox1 (1:1000; catalog 10957-1-AP), and GNPAT (1:1000; catalog 14931-1-AP) were from Proteintech.

    Techniques: Injection