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16837 1 ap  (Proteintech)


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    Proteintech 16837 1 ap
    16837 1 Ap, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 282 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/alkbh5/ALKBH5+Antibody/pmc13040171-10-2-6
    Average 96 stars, based on 282 article reviews
    16837 1 ap - by Bioz Stars, 2026-10
    96/100 stars

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    Related Articles

    other:

    Article Title: m6A Modification of ATOX1 Inhibits Acute Myeloid Leukemia Progression by Promoting Cuproptosis
    Article Snippet: ALKBH5 , 16837-1-AP , 1:5,000 , Proteintech , AB_2242665.

    Article Title: m6A RNA methylation modulates antiviral response in celiac disease.
    Article Snippet: Following Genes & Immunity electrophoresis, proteins were transferred onto nitrocellulose membranes using a Transblot-Turbo Transfer System (BioRad) and blocked in 5% nonfatty milk diluted in TBST 1X (20mM Tris, 150mM NaCl and 0.1% Tween 20) at room temperature for 1 h. The membranes were incubated overnight at 4 °C with primary antibodies at a 1:1000 dilution.

    Western Blot:

    Article Title: METTL3-mediated m6A modification of FDX1 confers resistance to cuproptosis and promotes hepatocellular carcinoma progression.
    Article Snippet: Supplemented with 10% fetal bovine serum (FBS, ExCell Bio, Shanghai, China). .. The following commercially available antibodies were used for Western blotting: GAPDH (Proteintech, 60004-4-lg), Flag-Tag (Abmart, TT0053), Myc-Tag (Abmart, M20002), METTL3 (Proteintech, 15073-1-AP), METTL14 (Abmart, PC17608), WTAP (Abmart, PA6128), FTO (Abmart, PA2776 ), ALKBH5 (Proteintech, 16837-1-AP), FDX1 (Abmart, ab108257), FMR1 (Proteintech, 13755-1-AP), DLAT (CST, 12362), YTHDF1 (Abmart, P55973R5), YTHDF2 (Abmart, PY100053), YTHDF3 (Abmart, PS05805), YTHDC1(Proteintech, 14392-1-AP), AR TI CL E IN P RE SS YTHDC2(Proteintech, 27779-1-AP), Lipoic acid antibody (Abcam, ab58724), m6A antibody (Synaptic Systems, 2002003). .. Ammonium tetrathiomolybdate (TTM) (Macklin, A828261), Elesclomol (Selleck, STA-4783), STM2457(Glpbio, GC19771), MitoTracker Red CMXRos (Thermo Fisher Scientific, M7512), Z-VAD-FMK (MCE, HY-16658B), 3-Methyladenine (Glpbio, GC10710), Ferrostatin-1 (Glpbio, GC10380).

    Article Title: Integrative Multi-Analysis Identifies METTL3-Regulated FGF19 and H6PD as Candidate Targets in Diabetic Cognitive Impairment
    Article Snippet: .. The following antibodies were used in this study: anti-GAPDH (Affinity BiosciencesCincinnati, OH, USA) (1:1000), anti-m 6 A (Synaptic Systems, Göttingen, Germany, 202003) (for Dot blot:1:1000, for IHC: 1:500), anti-METTL3 (15073-1-AP, Proteintech, Rosemont, Illinois, USA) (for WB:1:2000, for IHC: 1:750), anti-METTL14 (HPA038002, Sigma-Aldrich, St. Louis, MO, USA) (for WB:1:2000, for IHC: 1:1000), anti-WTAP (60188-1-Ig, Proteintech) (for WB:1:2000, for IHC: 1:500), FTO (27226-1-AP, Proteintech) (for WB:1:1000, for IHC: 1:400), ALKBH5 (16837-1-AP, Proteintech) (for WB:1:2000, for IHC: 1:200), Goat Anti-Mouse IgG H&L (HRP, Affinity Biosciences) (1:10000), Goat Anti-Rabbit IgG H&L (HRP, Affinity Biosciences, Cincinnati, OH, USA) (1:10000), and Goat Anti-Rabbit IgG H&L (Alexa Fluor 488, Abcam, Cambridge, UK) (1:500). .. Seven-week-old SPF-grade male C57BL/6 mice were obtained from Beijing Vital River Laboratory Animal Technology Co., Ltd. (Beijing, China) Male db/db (C57BLKS/J- leprdb/leprdb ) mice and age-matched wild-type db/m (C57BLKS/J- LepRdb/+ ) mice were obtained from the Model Animal Research Center of Nanjing University.

    Article Title: METTL3-mediated m6A modification of FDX1 confers resistance to cuproptosis and promotes hepatocellular carcinoma progression
    Article Snippet: Supplemented with 10% fetal bovine serum (FBS, ExCell Bio, Shanghai, China). .. The following commercially available antibodies were used for Western blotting: GAPDH (Proteintech, 60004-4-lg), Flag-Tag (Abmart, TT0053), Myc-Tag (Abmart, M20002 ), METTL3 (Proteintech, 15073-1-AP), METTL14 (Abmart, PC17608), WTAP (Abmart, PA6128), FTO (Abmart, PA2776), ALKBH5 (Proteintech, 16837-1-AP), FDX1 (Abmart, ab108257), FMR1 (Proteintech, 13755-1-AP), DLAT (CST, 12362), YTHDF1 (Abmart, P55973R5), YTHDF2 (Abmart, PY100053 ), YTHDF3 (Abmart, PS05805), YTHDC1(Proteintech, 14392-1-AP), YTHDC2(Proteintech, 27779-1-AP), Lipoic acid antibody (Abcam, ab58724), m6A antibody (Synaptic Systems, 2002003). .. Ammonium tetrathiomolybdate (TTM) (Macklin, A828261), Elesclomol (Selleck, STA-4783), STM2457(Glpbio, GC19771), MitoTracker Red CMXRos (Thermo Fisher Scientific, M7512), Z-VAD-FMK (MCE, HY-16658B), 3-Methyladenine (Glpbio, GC10710), Ferrostatin-1 (Glpbio, GC10380).

    Article Title: Integrative Multi-Analysis Identifies METTL3-Regulated FGF19 and H6PD as Candidate Targets in Diabetic Cognitive Impairment
    Article Snippet: .. The following antibodies were used in this study: anti-GAPDH (Affinity BiosciencesCincinnati, OH, USA) (1:1000), anti-m6A (Synaptic Systems, Göttingen, Germany, 202003) (for Dot blot:1:1000, for IHC: 1:500), anti-METTL3 (15073-1-AP, Proteintech, Rosemont, Illinois, USA) (for WB:1:2000, for IHC: 1:750), anti-METTL14 (HPA038002, SigmaAldrich, St. Louis, MO, USA) (for WB:1:2000, for IHC: 1:1000), anti-WTAP (60188-1-Ig, Proteintech) (for WB:1:2000, for IHC: 1:500), FTO (27226-1-AP, Proteintech) (for WB:1:1000, for IHC: 1:400), ALKBH5 (16837-1-AP, Proteintech) (for WB:1:2000, for IHC: 1:200), Goat Anti-Mouse IgG H&L (HRP, Affinity Biosciences) (1:10000), Goat Anti-Rabbit IgG H&L (HRP, Affinity Biosciences, Cincinnati, OH, USA) (1:10000), and Goat Anti-Rabbit IgG H&L (Alexa Fluor 488, Abcam, Cambridge, UK) (1:500). .. Seven-week-old SPF-grade male C57BL/6 mice were obtained from Beijing Vital River Laboratory Animal Technology Co., Ltd. (Beijing, China) Male db/db (C57BLKS/Jleprdb/leprdb) mice and age-matched wild-type db/m (C57BLKS/J-LepRdb/+) mice were obtained from the Model Animal Research Center of Nanjing University.

    Immunohistochemistry:

    Article Title: Integrative Multi-Analysis Identifies METTL3-Regulated FGF19 and H6PD as Candidate Targets in Diabetic Cognitive Impairment
    Article Snippet: .. The following antibodies were used in this study: anti-GAPDH (Affinity BiosciencesCincinnati, OH, USA) (1:1000), anti-m 6 A (Synaptic Systems, Göttingen, Germany, 202003) (for Dot blot:1:1000, for IHC: 1:500), anti-METTL3 (15073-1-AP, Proteintech, Rosemont, Illinois, USA) (for WB:1:2000, for IHC: 1:750), anti-METTL14 (HPA038002, Sigma-Aldrich, St. Louis, MO, USA) (for WB:1:2000, for IHC: 1:1000), anti-WTAP (60188-1-Ig, Proteintech) (for WB:1:2000, for IHC: 1:500), FTO (27226-1-AP, Proteintech) (for WB:1:1000, for IHC: 1:400), ALKBH5 (16837-1-AP, Proteintech) (for WB:1:2000, for IHC: 1:200), Goat Anti-Mouse IgG H&L (HRP, Affinity Biosciences) (1:10000), Goat Anti-Rabbit IgG H&L (HRP, Affinity Biosciences, Cincinnati, OH, USA) (1:10000), and Goat Anti-Rabbit IgG H&L (Alexa Fluor 488, Abcam, Cambridge, UK) (1:500). .. Seven-week-old SPF-grade male C57BL/6 mice were obtained from Beijing Vital River Laboratory Animal Technology Co., Ltd. (Beijing, China) Male db/db (C57BLKS/J- leprdb/leprdb ) mice and age-matched wild-type db/m (C57BLKS/J- LepRdb/+ ) mice were obtained from the Model Animal Research Center of Nanjing University.

    Article Title: Integrative Multi-Analysis Identifies METTL3-Regulated FGF19 and H6PD as Candidate Targets in Diabetic Cognitive Impairment
    Article Snippet: .. The following antibodies were used in this study: anti-GAPDH (Affinity BiosciencesCincinnati, OH, USA) (1:1000), anti-m6A (Synaptic Systems, Göttingen, Germany, 202003) (for Dot blot:1:1000, for IHC: 1:500), anti-METTL3 (15073-1-AP, Proteintech, Rosemont, Illinois, USA) (for WB:1:2000, for IHC: 1:750), anti-METTL14 (HPA038002, SigmaAldrich, St. Louis, MO, USA) (for WB:1:2000, for IHC: 1:1000), anti-WTAP (60188-1-Ig, Proteintech) (for WB:1:2000, for IHC: 1:500), FTO (27226-1-AP, Proteintech) (for WB:1:1000, for IHC: 1:400), ALKBH5 (16837-1-AP, Proteintech) (for WB:1:2000, for IHC: 1:200), Goat Anti-Mouse IgG H&L (HRP, Affinity Biosciences) (1:10000), Goat Anti-Rabbit IgG H&L (HRP, Affinity Biosciences, Cincinnati, OH, USA) (1:10000), and Goat Anti-Rabbit IgG H&L (Alexa Fluor 488, Abcam, Cambridge, UK) (1:500). .. Seven-week-old SPF-grade male C57BL/6 mice were obtained from Beijing Vital River Laboratory Animal Technology Co., Ltd. (Beijing, China) Male db/db (C57BLKS/Jleprdb/leprdb) mice and age-matched wild-type db/m (C57BLKS/J-LepRdb/+) mice were obtained from the Model Animal Research Center of Nanjing University.

    Blocking Assay:

    Article Title: Acupuncture Inhibits Ferroptosis to Attenuate Cerebral Ischemia-Reperfusion Injury Through FTO-Mediated m6A Modification of ACSL4.
    Article Snippet: Acupuncture, a traditional Chinese medical intervention, is extensively utilized in the management of ischemic stroke across its various stages.. However, the precise mechanisms underlying its therapeutic action are not fully elucidated.. The present study sought to investigate the therapeutic effects and unravel the potential mechanisms of Xingnao Kaiqiao (XNKQ) acupuncture in ameliorating cerebral ischemia-reperfusion injury (CIRI).

    Membrane:

    Article Title: Acupuncture Inhibits Ferroptosis to Attenuate Cerebral Ischemia-Reperfusion Injury Through FTO-Mediated m6A Modification of ACSL4.
    Article Snippet: Acupuncture, a traditional Chinese medical intervention, is extensively utilized in the management of ischemic stroke across its various stages.. However, the precise mechanisms underlying its therapeutic action are not fully elucidated.. The present study sought to investigate the therapeutic effects and unravel the potential mechanisms of Xingnao Kaiqiao (XNKQ) acupuncture in ameliorating cerebral ischemia-reperfusion injury (CIRI).

    Incubation:

    Article Title: Acupuncture Inhibits Ferroptosis to Attenuate Cerebral Ischemia-Reperfusion Injury Through FTO-Mediated m6A Modification of ACSL4.
    Article Snippet: Acupuncture, a traditional Chinese medical intervention, is extensively utilized in the management of ischemic stroke across its various stages.. However, the precise mechanisms underlying its therapeutic action are not fully elucidated.. The present study sought to investigate the therapeutic effects and unravel the potential mechanisms of Xingnao Kaiqiao (XNKQ) acupuncture in ameliorating cerebral ischemia-reperfusion injury (CIRI).



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    Image Search Results


    ATOX1 expression is affected by ALKBH5-mediated modification of m6A methylation. A, RNA pull-down assay for identifying the interaction of ATOX1 RNA with METTL3, ALKBH5, ELAVL1, and HNRNPC. AML cells were transfected with oe-NC or oe- ALKBH5 . B, RIP-qPCR assay for detecting the m6A methylation level of ATOX1 in AML cells. C, qRT-PCR of ATOX1 transcripts in ActD-treated AML cells. D, Western blot analysis of ATOX1 expression in AML cells. AML cells were transfected with sh-NC or sh- ALKBH5 . E, Western blot analysis of ATOX1 expression in AML cells. Data are shown as mean ± SD. n = 3.

    Journal: Cancer Research Communications

    Article Title: m6A Modification of ATOX1 Inhibits Acute Myeloid Leukemia Progression by Promoting Cuproptosis

    doi: 10.1158/2767-9764.CRC-25-0436

    Figure Lengend Snippet: ATOX1 expression is affected by ALKBH5-mediated modification of m6A methylation. A, RNA pull-down assay for identifying the interaction of ATOX1 RNA with METTL3, ALKBH5, ELAVL1, and HNRNPC. AML cells were transfected with oe-NC or oe- ALKBH5 . B, RIP-qPCR assay for detecting the m6A methylation level of ATOX1 in AML cells. C, qRT-PCR of ATOX1 transcripts in ActD-treated AML cells. D, Western blot analysis of ATOX1 expression in AML cells. AML cells were transfected with sh-NC or sh- ALKBH5 . E, Western blot analysis of ATOX1 expression in AML cells. Data are shown as mean ± SD. n = 3.

    Article Snippet: ALKBH5 , 16837-1-AP , 1:5,000 , Proteintech , AB_2242665.

    Techniques: Expressing, Modification, Methylation, Pull Down Assay, Transfection, Quantitative RT-PCR, Western Blot

    ALKBH5-mediated m6A modification regulating ATOX1 expression affects cuproptosis in AML cells. AML cells transfected with oe- ATOX1 and/or oe- ALKBH5 were treated with 200 nmol/L ES/Cu for 72 hours. A, Western blot analysis of ATOX1 and ALKBH5 expression in AML cells. B, CCK-8 assay for detecting the viability of AML cells. C, EDU staining assay for detecting the cell proliferation of AML cells. Scale bar, 25 μm. D, Flow cytometry for detecting the cell death of AML cells. E, Western blot analysis of lipoylated DLAT expression in AML cells. F, Western blot analysis of Fe–S cluster protein (FDX1, LIAS, and ACO2) expression in AML cells. Data are shown as mean ± SD. n = 3. SSC, side scatter.

    Journal: Cancer Research Communications

    Article Title: m6A Modification of ATOX1 Inhibits Acute Myeloid Leukemia Progression by Promoting Cuproptosis

    doi: 10.1158/2767-9764.CRC-25-0436

    Figure Lengend Snippet: ALKBH5-mediated m6A modification regulating ATOX1 expression affects cuproptosis in AML cells. AML cells transfected with oe- ATOX1 and/or oe- ALKBH5 were treated with 200 nmol/L ES/Cu for 72 hours. A, Western blot analysis of ATOX1 and ALKBH5 expression in AML cells. B, CCK-8 assay for detecting the viability of AML cells. C, EDU staining assay for detecting the cell proliferation of AML cells. Scale bar, 25 μm. D, Flow cytometry for detecting the cell death of AML cells. E, Western blot analysis of lipoylated DLAT expression in AML cells. F, Western blot analysis of Fe–S cluster protein (FDX1, LIAS, and ACO2) expression in AML cells. Data are shown as mean ± SD. n = 3. SSC, side scatter.

    Article Snippet: ALKBH5 , 16837-1-AP , 1:5,000 , Proteintech , AB_2242665.

    Techniques: Modification, Expressing, Transfection, Western Blot, CCK-8 Assay, Staining, Flow Cytometry

    Animal experiments validate the therapeutic potential of the ALKBH5–ATOX1 axis for AML. Female BALB/c nude mice were subcutaneously injected with 1 × 10 7 NOMO-1 cells in the right axilla. A, Western blot analysis of ATOX1 and ALKBH5 expression in tumor tissues of AML model mice. B, The growth curve of tumor volume in AML model mice. C, Representative images and weight of tumors in AML. D and E, IHC assay for detecting Ki67 expression. Scale bar, 25 and 100 μm. F, Western blot analysis of lipoylated DLAT expression in tumor tissues of AML model mice. G, Western blot analysis of Fe–S cluster protein (FDX1 and LIAS) expression in tumor tissues of AML model mice. Data are shown as mean ± SD. n = 5.

    Journal: Cancer Research Communications

    Article Title: m6A Modification of ATOX1 Inhibits Acute Myeloid Leukemia Progression by Promoting Cuproptosis

    doi: 10.1158/2767-9764.CRC-25-0436

    Figure Lengend Snippet: Animal experiments validate the therapeutic potential of the ALKBH5–ATOX1 axis for AML. Female BALB/c nude mice were subcutaneously injected with 1 × 10 7 NOMO-1 cells in the right axilla. A, Western blot analysis of ATOX1 and ALKBH5 expression in tumor tissues of AML model mice. B, The growth curve of tumor volume in AML model mice. C, Representative images and weight of tumors in AML. D and E, IHC assay for detecting Ki67 expression. Scale bar, 25 and 100 μm. F, Western blot analysis of lipoylated DLAT expression in tumor tissues of AML model mice. G, Western blot analysis of Fe–S cluster protein (FDX1 and LIAS) expression in tumor tissues of AML model mice. Data are shown as mean ± SD. n = 5.

    Article Snippet: ALKBH5 , 16837-1-AP , 1:5,000 , Proteintech , AB_2242665.

    Techniques: Injection, Western Blot, Expressing

    Schematic illustration of the proposed mechanisms: As depicted, ATOX1 undergoes m6A modification mediated by ALKBH5, which is upregulated in AML. This posttranscriptional modification destabilizes ATOX1 mRNA, leading to reduced ATOX1 expression. Consequently, the suppression of cuproptosis in AML cells is alleviated, thereby promoting AML progression.

    Journal: Cancer Research Communications

    Article Title: m6A Modification of ATOX1 Inhibits Acute Myeloid Leukemia Progression by Promoting Cuproptosis

    doi: 10.1158/2767-9764.CRC-25-0436

    Figure Lengend Snippet: Schematic illustration of the proposed mechanisms: As depicted, ATOX1 undergoes m6A modification mediated by ALKBH5, which is upregulated in AML. This posttranscriptional modification destabilizes ATOX1 mRNA, leading to reduced ATOX1 expression. Consequently, the suppression of cuproptosis in AML cells is alleviated, thereby promoting AML progression.

    Article Snippet: ALKBH5 , 16837-1-AP , 1:5,000 , Proteintech , AB_2242665.

    Techniques: Modification, Expressing