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  • 94
    New England Biolabs pspxi
    Pspxi, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pspxi/product/New England Biolabs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    pspxi - by Bioz Stars, 2022-08
    94/100 stars
      Buy from Supplier

    95
    Millipore anti rab14 c terminal antibody
    The binding of CPT1A to <t>Rab14</t> is enhanced in radiation-resistant NPC cells, which might promote the contact of lipid droplet and mitochondria in these cells. (A) Immunoprecipitation analysis showing the binding of CPT1A and Rab14 in CNE2-IR and HK1-IR compared with parental cells. IgG served as a negative control. (B) Immunoprecipitation analysis showing the binding of CPT1A and Rab14 in CNE2 and HK1 cells stably expressing CPT1A-V5 or empty vector. IgG served as a negative control. (C) Proximity ligation assay indicating the interaction of CPT1A and Rab14 in CNE2-IR and HK1-IR compared with parental cells at 24 h after exposure to 4 Gy IR (red: PLA positive signal; blue: DAPI, scale bar = 25 μm). (D) Based on the prediction of Fd-DCA, the N terminal of CPT1A was found to bind with the identified Site 2 of Rab14 ( left ) and the predicted top 20 strongest coupled interacting residue pairs (interacting residue contacts) of these two proteins (orange stick bonds, right ). (E) Immunoblot analysis showing translocation of CPT1A to mitochondria in CNE2 and CNE2-IR cells transfected with a Rab14 siRNA pool or negative siRNA at 24 h after exposure to 4 Gy IR. β-Actin was used as a control to confirm equal loading of protein and Hsp60 served as a control to confirm equal loading of mitochondrial fractions. (F) Confocal microscopy analysis of the co-localization of Rab14 and lipid droplets in CNE2-IR and HK1-IR cells and parental cells at 24 h after exposure to 4 Gy IR (red: Ra b14; green: BODIPY 493/503; blue: DAPI; scale bar = 25 μm). (G) Confocal microscopy analysis of the co-localization of CPT1A, Rab14 and mitochondria in the groups indicated in (F) (red: Rab14; green: BODIPY 493/503; blue: DAPI; scale bar = 25 μm).
    Anti Rab14 C Terminal Antibody, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti rab14 c terminal antibody/product/Millipore
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti rab14 c terminal antibody - by Bioz Stars, 2022-08
    95/100 stars
      Buy from Supplier

    Image Search Results


    The binding of CPT1A to Rab14 is enhanced in radiation-resistant NPC cells, which might promote the contact of lipid droplet and mitochondria in these cells. (A) Immunoprecipitation analysis showing the binding of CPT1A and Rab14 in CNE2-IR and HK1-IR compared with parental cells. IgG served as a negative control. (B) Immunoprecipitation analysis showing the binding of CPT1A and Rab14 in CNE2 and HK1 cells stably expressing CPT1A-V5 or empty vector. IgG served as a negative control. (C) Proximity ligation assay indicating the interaction of CPT1A and Rab14 in CNE2-IR and HK1-IR compared with parental cells at 24 h after exposure to 4 Gy IR (red: PLA positive signal; blue: DAPI, scale bar = 25 μm). (D) Based on the prediction of Fd-DCA, the N terminal of CPT1A was found to bind with the identified Site 2 of Rab14 ( left ) and the predicted top 20 strongest coupled interacting residue pairs (interacting residue contacts) of these two proteins (orange stick bonds, right ). (E) Immunoblot analysis showing translocation of CPT1A to mitochondria in CNE2 and CNE2-IR cells transfected with a Rab14 siRNA pool or negative siRNA at 24 h after exposure to 4 Gy IR. β-Actin was used as a control to confirm equal loading of protein and Hsp60 served as a control to confirm equal loading of mitochondrial fractions. (F) Confocal microscopy analysis of the co-localization of Rab14 and lipid droplets in CNE2-IR and HK1-IR cells and parental cells at 24 h after exposure to 4 Gy IR (red: Ra b14; green: BODIPY 493/503; blue: DAPI; scale bar = 25 μm). (G) Confocal microscopy analysis of the co-localization of CPT1A, Rab14 and mitochondria in the groups indicated in (F) (red: Rab14; green: BODIPY 493/503; blue: DAPI; scale bar = 25 μm).

    Journal: Theranostics

    Article Title: Targeting CPT1A-mediated fatty acid oxidation sensitizes nasopharyngeal carcinoma to radiation therapy

    doi: 10.7150/thno.21451

    Figure Lengend Snippet: The binding of CPT1A to Rab14 is enhanced in radiation-resistant NPC cells, which might promote the contact of lipid droplet and mitochondria in these cells. (A) Immunoprecipitation analysis showing the binding of CPT1A and Rab14 in CNE2-IR and HK1-IR compared with parental cells. IgG served as a negative control. (B) Immunoprecipitation analysis showing the binding of CPT1A and Rab14 in CNE2 and HK1 cells stably expressing CPT1A-V5 or empty vector. IgG served as a negative control. (C) Proximity ligation assay indicating the interaction of CPT1A and Rab14 in CNE2-IR and HK1-IR compared with parental cells at 24 h after exposure to 4 Gy IR (red: PLA positive signal; blue: DAPI, scale bar = 25 μm). (D) Based on the prediction of Fd-DCA, the N terminal of CPT1A was found to bind with the identified Site 2 of Rab14 ( left ) and the predicted top 20 strongest coupled interacting residue pairs (interacting residue contacts) of these two proteins (orange stick bonds, right ). (E) Immunoblot analysis showing translocation of CPT1A to mitochondria in CNE2 and CNE2-IR cells transfected with a Rab14 siRNA pool or negative siRNA at 24 h after exposure to 4 Gy IR. β-Actin was used as a control to confirm equal loading of protein and Hsp60 served as a control to confirm equal loading of mitochondrial fractions. (F) Confocal microscopy analysis of the co-localization of Rab14 and lipid droplets in CNE2-IR and HK1-IR cells and parental cells at 24 h after exposure to 4 Gy IR (red: Ra b14; green: BODIPY 493/503; blue: DAPI; scale bar = 25 μm). (G) Confocal microscopy analysis of the co-localization of CPT1A, Rab14 and mitochondria in the groups indicated in (F) (red: Rab14; green: BODIPY 493/503; blue: DAPI; scale bar = 25 μm).

    Article Snippet: Antibodies included anti-CPT1A, anti-cleaved caspase 9, anti-MLKL (phospho S358) (Abcam, MA, USA), anti-cleaved-PARP, anti-cleaved caspase 3, anti-normal rabbit IgG and anti-normal mouse IgG (Cell Signaling Technologies, MA, USA), anti-Rab14, anti-Rab7A, anti-MLKL and anti-β-actin (Sigma-Aldrich, Darmstadt, Germany), anti-HSP60 (Santa Cruz, CA, USA), and anti-LC3 I/II (Novus Biologicals, CA, USA).

    Techniques: Binding Assay, Immunoprecipitation, Negative Control, Stable Transfection, Expressing, Plasmid Preparation, Proximity Ligation Assay, Translocation Assay, Transfection, Confocal Microscopy

    Etomoxir decreases the binding of CPT1A and Rab14, which attenuates fatty acid trafficking in radiation-resistant NPC cells. (A) Immunoprecipitation analysis showing the binding of CPT1A and Rab14 in CNE2-IR and HK1-IR compared with parental cells at 24 h after exposure to 4 Gy IR or Etomoxir (80 μM). IgG served as a negative control. (B) Confocal microscopy analysis of morphologies and subcellular location of free fatty acids in groups indicated in (A) (red: Mito Tracker Red; green: BODIPY C16; blue: DAPI; scale bar = 25 μm). (C) Pearson's coefficient analysis representing relative cellular co-localization of free fatty acids overlapping with mitochondria in groups indicated in (A). Images were analyzed using Image J software. Data are expressed as mean values ± S.D. of 12 independent cells analyzed by microscopy for each group (* p

    Journal: Theranostics

    Article Title: Targeting CPT1A-mediated fatty acid oxidation sensitizes nasopharyngeal carcinoma to radiation therapy

    doi: 10.7150/thno.21451

    Figure Lengend Snippet: Etomoxir decreases the binding of CPT1A and Rab14, which attenuates fatty acid trafficking in radiation-resistant NPC cells. (A) Immunoprecipitation analysis showing the binding of CPT1A and Rab14 in CNE2-IR and HK1-IR compared with parental cells at 24 h after exposure to 4 Gy IR or Etomoxir (80 μM). IgG served as a negative control. (B) Confocal microscopy analysis of morphologies and subcellular location of free fatty acids in groups indicated in (A) (red: Mito Tracker Red; green: BODIPY C16; blue: DAPI; scale bar = 25 μm). (C) Pearson's coefficient analysis representing relative cellular co-localization of free fatty acids overlapping with mitochondria in groups indicated in (A). Images were analyzed using Image J software. Data are expressed as mean values ± S.D. of 12 independent cells analyzed by microscopy for each group (* p

    Article Snippet: Antibodies included anti-CPT1A, anti-cleaved caspase 9, anti-MLKL (phospho S358) (Abcam, MA, USA), anti-cleaved-PARP, anti-cleaved caspase 3, anti-normal rabbit IgG and anti-normal mouse IgG (Cell Signaling Technologies, MA, USA), anti-Rab14, anti-Rab7A, anti-MLKL and anti-β-actin (Sigma-Aldrich, Darmstadt, Germany), anti-HSP60 (Santa Cruz, CA, USA), and anti-LC3 I/II (Novus Biologicals, CA, USA).

    Techniques: Binding Assay, Immunoprecipitation, Negative Control, Confocal Microscopy, Software, Microscopy

    A schematic to illustrate CPT1A-mediated radiation resistance in NPC. (A) The enhanced CPT1A expression and the CPT1A-Rab14 interaction promote fatty acid trafficking between lipid droplets and mitochondria, which facilitates fatty acid utilization and maximizes ATP production, leading to resistance to radiation. (B) Blockage of CPT1A attenuates fatty acid trafficking and FAO, causes lipid accumulation and energy stress, which induces mitochondrial apoptosis and re-sensitizes NPC cells to radiation.

    Journal: Theranostics

    Article Title: Targeting CPT1A-mediated fatty acid oxidation sensitizes nasopharyngeal carcinoma to radiation therapy

    doi: 10.7150/thno.21451

    Figure Lengend Snippet: A schematic to illustrate CPT1A-mediated radiation resistance in NPC. (A) The enhanced CPT1A expression and the CPT1A-Rab14 interaction promote fatty acid trafficking between lipid droplets and mitochondria, which facilitates fatty acid utilization and maximizes ATP production, leading to resistance to radiation. (B) Blockage of CPT1A attenuates fatty acid trafficking and FAO, causes lipid accumulation and energy stress, which induces mitochondrial apoptosis and re-sensitizes NPC cells to radiation.

    Article Snippet: Antibodies included anti-CPT1A, anti-cleaved caspase 9, anti-MLKL (phospho S358) (Abcam, MA, USA), anti-cleaved-PARP, anti-cleaved caspase 3, anti-normal rabbit IgG and anti-normal mouse IgG (Cell Signaling Technologies, MA, USA), anti-Rab14, anti-Rab7A, anti-MLKL and anti-β-actin (Sigma-Aldrich, Darmstadt, Germany), anti-HSP60 (Santa Cruz, CA, USA), and anti-LC3 I/II (Novus Biologicals, CA, USA).

    Techniques: Expressing

    Knockdown of Rab14 re-sensitizes CPT1A-overexpressing NPC cells to radiation therapy, suppresses fatty acid trafficking from lipid droplets into mitochondria and induces accumulation of lipid droplets in these cells. (A) Colony formation assay showing survival fractions of CNE2-EV, CNE2-CPT1A, HK1-EV and HK1-CPT1A cells transfected with a Rab14 siRNA pool or negative siRNA after exposure to 4 Gy IR. Survival fractions were calculated by comparing the colony number of each treatment group with untreated groups. Results are plotted as the mean survival fraction ± S.D. of 3 independent experiments (* p

    Journal: Theranostics

    Article Title: Targeting CPT1A-mediated fatty acid oxidation sensitizes nasopharyngeal carcinoma to radiation therapy

    doi: 10.7150/thno.21451

    Figure Lengend Snippet: Knockdown of Rab14 re-sensitizes CPT1A-overexpressing NPC cells to radiation therapy, suppresses fatty acid trafficking from lipid droplets into mitochondria and induces accumulation of lipid droplets in these cells. (A) Colony formation assay showing survival fractions of CNE2-EV, CNE2-CPT1A, HK1-EV and HK1-CPT1A cells transfected with a Rab14 siRNA pool or negative siRNA after exposure to 4 Gy IR. Survival fractions were calculated by comparing the colony number of each treatment group with untreated groups. Results are plotted as the mean survival fraction ± S.D. of 3 independent experiments (* p

    Article Snippet: Antibodies included anti-CPT1A, anti-cleaved caspase 9, anti-MLKL (phospho S358) (Abcam, MA, USA), anti-cleaved-PARP, anti-cleaved caspase 3, anti-normal rabbit IgG and anti-normal mouse IgG (Cell Signaling Technologies, MA, USA), anti-Rab14, anti-Rab7A, anti-MLKL and anti-β-actin (Sigma-Aldrich, Darmstadt, Germany), anti-HSP60 (Santa Cruz, CA, USA), and anti-LC3 I/II (Novus Biologicals, CA, USA).

    Techniques: Colony Assay, Transfection