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anti mt atp6  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc anti mt atp6
    Anti Mt Atp6, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+mt+atp6/MT-ATP6+Antibody/pmc12925242-3-0-2
    Average 94 stars, based on 13 article reviews
    anti mt atp6 - by Bioz Stars, 2026-10
    94/100 stars

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    Related Articles

    Cell-Signaling:

    Article Title: Reversible dissociation of mitochondrial Complex V balances anabolic and energy-generating needs in cancer
    Article Snippet: Anti-ATP5FA1 , Cell Signaling Technology, Inc , cat#18023; RRID: AB_2925225. .. Anti-MT-ATP6 , Cell Signaling Technology, Inc , cat#70262. .. Anti-V5 epitope , ThermoFisher , cat#46-07-05.

    other:

    Article Title: Selection of initiator tRNA and start codon by mammalian mitochondrial initiation factor 3 in leaderless mRNA translation
    Article Snippet: For standardization, the gels were stained with GelCode Blue Safe Protein Stain (Thermo Fisher Scientific) to monitor the protein input using the IR 700-nm channel.



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    A Procedures for subcutaneous tumour model establishment in KG1a mice. KG1a cells transfected with the empty vector lentivirus or the ALDH2-overexpression vector were subcutaneously injected into NCG mice (5 × 10 6 cells per mouse). After 30 days, the cells were given an intraperitoneal injection of 60 mg/kg Ara-C and/or 7.5 mg/kg CVT-10216 or PBS (3 times a week) for an additional 10 days. B The appearance of subcutaneous tumour tissue in each mouse group. C Overall survival of each treated mouse ( n = 4 mice per group). P -values were calculated with the log-rank test. **: p < 0.01. D Weights of the mice in each group. E , F Immunohistochemical staining and histograms of subcutaneous tumour tissue samples showing the coexpression proportions of ALDH2- and Mito-positive cells. G , H The volume curves ( H ) and weights ( G ) of the subcutaneous tumour tissue in each group are shown. I , J HE-stained sections ( I ) of the subcutaneous tumour tissue from each mouse group and immunohistochemical staining of ALDH2, MT-CO1, MT-ND5 and <t>MT-ATP6</t> ( J ) in the subcutaneous tumour tissue sections (each group of 20 images was analysed, n = 4 mice per group).
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    A Procedures for subcutaneous tumour model establishment in KG1a mice. KG1a cells transfected with the empty vector lentivirus or the ALDH2-overexpression vector were subcutaneously injected into NCG mice (5 × 10 6 cells per mouse). After 30 days, the cells were given an intraperitoneal injection of 60 mg/kg Ara-C and/or 7.5 mg/kg CVT-10216 or PBS (3 times a week) for an additional 10 days. B The appearance of subcutaneous tumour tissue in each mouse group. C Overall survival of each treated mouse ( n = 4 mice per group). P -values were calculated with the log-rank test. **: p < 0.01. D Weights of the mice in each group. E , F Immunohistochemical staining and histograms of subcutaneous tumour tissue samples showing the coexpression proportions of ALDH2- and Mito-positive cells. G , H The volume curves ( H ) and weights ( G ) of the subcutaneous tumour tissue in each group are shown. I , J HE-stained sections ( I ) of the subcutaneous tumour tissue from each mouse group and immunohistochemical staining of ALDH2, MT-CO1, MT-ND5 and <t>MT-ATP6</t> ( J ) in the subcutaneous tumour tissue sections (each group of 20 images was analysed, n = 4 mice per group).
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    Huabio Inc mt atp6
    Mechanism of anti-DLBCL action of MM-Lipid@Vpz. ( A ) Intersection of two sample genes by using Venn diagram. The Orange part is group Lipid@Vpz, the blue part is group MM-Lipid@Vpz. Intersections are genes that are the same in both samples. ( B ) KEGG enrichment analysis of signaling pathways. ( C ) Enrichment chordal maps visualize the signaling pathways and differential genes enriched in both samples. ( D ) Generating heat maps from differentially oxidatively phosphorylated genes. ( E ) Western blot analysis of MT-ND5, MT-CYB, MT-CO3 and <t>MT-ATP6</t> expression in each group. ( F ) Volcano plot showing representative differential genes.
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    Cell Signaling Technology Inc rabbit anti mt atp6 antibody
    Fig. 3. Combination of HANP/GKT831 inhibited tumor progression and impacted metabolism with radiotherapy. HANP/GKT831 enhanced sensitivity to radiation and suppressed cell migration and invasion in the MC38 mouse tumor cells. A. Colony formation assay detected cell colonies resistant to 2 Gy of RT (n = 3). B. Transwell migration assay evaluated cell migration following the treatments. Cells were treated with 0.01 μM of conventional GKT831 or HANP/GKT831 con taining 0.01 μM of equivalent doses of GKT831. Quantification of 2D migration assay after 48 h in culture (n = 5). HANP/GKT831 reduced the protein levels of representative signal molecules in glycolysis, mitochondrial OXPHOS, and DNA repair pathways. C. The levels of Western blot analysis of NOX1, NOX4, glycolysis related (Hexokinase 2 and PKM2), and mitochondrial OXPHOS associated proteins <t>(MT-ATP6</t> and MT-ND1). D. The protein levels in the cell cycle and DNA repair pathway, Cyclin D1, MSH6, and CHK1 proteins, were examined from the treated tumor lysates by Western blot analysis. β-actin served as the loading control. Similar results were obtained from at least 3 repeated studies. Student’s t-test: *p < 0.05 and ****p < 0.0001.
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    Image Search Results


    A Procedures for subcutaneous tumour model establishment in KG1a mice. KG1a cells transfected with the empty vector lentivirus or the ALDH2-overexpression vector were subcutaneously injected into NCG mice (5 × 10 6 cells per mouse). After 30 days, the cells were given an intraperitoneal injection of 60 mg/kg Ara-C and/or 7.5 mg/kg CVT-10216 or PBS (3 times a week) for an additional 10 days. B The appearance of subcutaneous tumour tissue in each mouse group. C Overall survival of each treated mouse ( n = 4 mice per group). P -values were calculated with the log-rank test. **: p < 0.01. D Weights of the mice in each group. E , F Immunohistochemical staining and histograms of subcutaneous tumour tissue samples showing the coexpression proportions of ALDH2- and Mito-positive cells. G , H The volume curves ( H ) and weights ( G ) of the subcutaneous tumour tissue in each group are shown. I , J HE-stained sections ( I ) of the subcutaneous tumour tissue from each mouse group and immunohistochemical staining of ALDH2, MT-CO1, MT-ND5 and MT-ATP6 ( J ) in the subcutaneous tumour tissue sections (each group of 20 images was analysed, n = 4 mice per group).

    Journal: Cell Death & Disease

    Article Title: The ALDH2/PolG2 axis enhances mitochondrial biogenesis via transcriptional regulation of Nrf2 and promotes chemotherapy resistance in acute myeloid leukaemia

    doi: 10.1038/s41419-025-07927-z

    Figure Lengend Snippet: A Procedures for subcutaneous tumour model establishment in KG1a mice. KG1a cells transfected with the empty vector lentivirus or the ALDH2-overexpression vector were subcutaneously injected into NCG mice (5 × 10 6 cells per mouse). After 30 days, the cells were given an intraperitoneal injection of 60 mg/kg Ara-C and/or 7.5 mg/kg CVT-10216 or PBS (3 times a week) for an additional 10 days. B The appearance of subcutaneous tumour tissue in each mouse group. C Overall survival of each treated mouse ( n = 4 mice per group). P -values were calculated with the log-rank test. **: p < 0.01. D Weights of the mice in each group. E , F Immunohistochemical staining and histograms of subcutaneous tumour tissue samples showing the coexpression proportions of ALDH2- and Mito-positive cells. G , H The volume curves ( H ) and weights ( G ) of the subcutaneous tumour tissue in each group are shown. I , J HE-stained sections ( I ) of the subcutaneous tumour tissue from each mouse group and immunohistochemical staining of ALDH2, MT-CO1, MT-ND5 and MT-ATP6 ( J ) in the subcutaneous tumour tissue sections (each group of 20 images was analysed, n = 4 mice per group).

    Article Snippet: Ara-C (HY-13605), Alda-1 (HY-18936) and CVT-10216 (HY-19801) antibodies were purchased from MedChemExpress Co., Ltd. ALDH2, Nrf2, MT-CO1, MT-ND5, MT-ATP6, ATPAF1, COX6A1, NDUFA6, CXCR4, BCL2, HO-1, ID1, Slc44a1, PolG2, PARP-1, cleaved PARP-1, CAS3, cleaved CAS3, γ-H2AX, LC3b and β-actin antibodies were purchased from AFFINIGY, Immunoway or ProteinTech (See Supplementary Table for details).

    Techniques: Transfection, Plasmid Preparation, Over Expression, Injection, Immunohistochemical staining, Staining

    Mechanism of anti-DLBCL action of MM-Lipid@Vpz. ( A ) Intersection of two sample genes by using Venn diagram. The Orange part is group Lipid@Vpz, the blue part is group MM-Lipid@Vpz. Intersections are genes that are the same in both samples. ( B ) KEGG enrichment analysis of signaling pathways. ( C ) Enrichment chordal maps visualize the signaling pathways and differential genes enriched in both samples. ( D ) Generating heat maps from differentially oxidatively phosphorylated genes. ( E ) Western blot analysis of MT-ND5, MT-CYB, MT-CO3 and MT-ATP6 expression in each group. ( F ) Volcano plot showing representative differential genes.

    Journal: International Journal of Nanomedicine

    Article Title: Macrophage Membrane-Coated Liposomes Delivering Vonoprazan Disrupt Mitochondrial Oxidative Phosphorylation in Diffuse Large B-Cell Lymphoma

    doi: 10.2147/IJN.S520567

    Figure Lengend Snippet: Mechanism of anti-DLBCL action of MM-Lipid@Vpz. ( A ) Intersection of two sample genes by using Venn diagram. The Orange part is group Lipid@Vpz, the blue part is group MM-Lipid@Vpz. Intersections are genes that are the same in both samples. ( B ) KEGG enrichment analysis of signaling pathways. ( C ) Enrichment chordal maps visualize the signaling pathways and differential genes enriched in both samples. ( D ) Generating heat maps from differentially oxidatively phosphorylated genes. ( E ) Western blot analysis of MT-ND5, MT-CYB, MT-CO3 and MT-ATP6 expression in each group. ( F ) Volcano plot showing representative differential genes.

    Article Snippet: The antibodies were detected by immunoblotting as follows:CCR2 (MCE, HY- P80385 ); E-Cadherin (Abcam, ab314063); Tublin (Selleck, F0167); Bcl-2 (ABclonal, A20777); Caspase3 (Selleck, F1080); Cleaved-Caspase3 (Selleck, F0135); MT-ND5 (HUABIO, #ER1913-30); MT-ATP6 (HUABIO, #ER60496); MT-CYB (ABclonal, A9762); MT-CO3 (Abcam, ab110259).

    Techniques: Protein-Protein interactions, Western Blot, Expressing

    The anti-DLBCL mechanism of MM-Lipid@Vpz in vivo ( A ) TUNEL staining of mouse tumor tissue, scale bars are 50 μm. ( B ) Western blot analysis of apoptosis-related proteins in tumor tissues of the control, Vpz, Lipid@Vpz, and MM-Lipid@Vpz groups. ( C ) ROS staining of mouse tumor tissue, scale bars are 50 μm. ( D ) The immunohistochemical analysis of the expression levels of MT-ND5, MT-CYB, MT-CO3 and MT-ATP6 in each group of tumor tissues, scale bars are 50 μm. ( E ) Western blot analysis of the expression levels of MT-ND5, MT-CYB, MT-CO3 and MT-ATP6 in each group of tumor tissues.

    Journal: International Journal of Nanomedicine

    Article Title: Macrophage Membrane-Coated Liposomes Delivering Vonoprazan Disrupt Mitochondrial Oxidative Phosphorylation in Diffuse Large B-Cell Lymphoma

    doi: 10.2147/IJN.S520567

    Figure Lengend Snippet: The anti-DLBCL mechanism of MM-Lipid@Vpz in vivo ( A ) TUNEL staining of mouse tumor tissue, scale bars are 50 μm. ( B ) Western blot analysis of apoptosis-related proteins in tumor tissues of the control, Vpz, Lipid@Vpz, and MM-Lipid@Vpz groups. ( C ) ROS staining of mouse tumor tissue, scale bars are 50 μm. ( D ) The immunohistochemical analysis of the expression levels of MT-ND5, MT-CYB, MT-CO3 and MT-ATP6 in each group of tumor tissues, scale bars are 50 μm. ( E ) Western blot analysis of the expression levels of MT-ND5, MT-CYB, MT-CO3 and MT-ATP6 in each group of tumor tissues.

    Article Snippet: The antibodies were detected by immunoblotting as follows:CCR2 (MCE, HY- P80385 ); E-Cadherin (Abcam, ab314063); Tublin (Selleck, F0167); Bcl-2 (ABclonal, A20777); Caspase3 (Selleck, F1080); Cleaved-Caspase3 (Selleck, F0135); MT-ND5 (HUABIO, #ER1913-30); MT-ATP6 (HUABIO, #ER60496); MT-CYB (ABclonal, A9762); MT-CO3 (Abcam, ab110259).

    Techniques: In Vivo, TUNEL Assay, Staining, Western Blot, Control, Immunohistochemical staining, Expressing

    Fig. 3. Combination of HANP/GKT831 inhibited tumor progression and impacted metabolism with radiotherapy. HANP/GKT831 enhanced sensitivity to radiation and suppressed cell migration and invasion in the MC38 mouse tumor cells. A. Colony formation assay detected cell colonies resistant to 2 Gy of RT (n = 3). B. Transwell migration assay evaluated cell migration following the treatments. Cells were treated with 0.01 μM of conventional GKT831 or HANP/GKT831 con taining 0.01 μM of equivalent doses of GKT831. Quantification of 2D migration assay after 48 h in culture (n = 5). HANP/GKT831 reduced the protein levels of representative signal molecules in glycolysis, mitochondrial OXPHOS, and DNA repair pathways. C. The levels of Western blot analysis of NOX1, NOX4, glycolysis related (Hexokinase 2 and PKM2), and mitochondrial OXPHOS associated proteins (MT-ATP6 and MT-ND1). D. The protein levels in the cell cycle and DNA repair pathway, Cyclin D1, MSH6, and CHK1 proteins, were examined from the treated tumor lysates by Western blot analysis. β-actin served as the loading control. Similar results were obtained from at least 3 repeated studies. Student’s t-test: *p < 0.05 and ****p < 0.0001.

    Journal: Biomaterials

    Article Title: Dual inhibition of oxidative phosphorylation and glycolysis using a hyaluronic acid nanoparticle NOX inhibitor enhanced response to radiotherapy in colorectal cancer.

    doi: 10.1016/j.biomaterials.2025.123437

    Figure Lengend Snippet: Fig. 3. Combination of HANP/GKT831 inhibited tumor progression and impacted metabolism with radiotherapy. HANP/GKT831 enhanced sensitivity to radiation and suppressed cell migration and invasion in the MC38 mouse tumor cells. A. Colony formation assay detected cell colonies resistant to 2 Gy of RT (n = 3). B. Transwell migration assay evaluated cell migration following the treatments. Cells were treated with 0.01 μM of conventional GKT831 or HANP/GKT831 con taining 0.01 μM of equivalent doses of GKT831. Quantification of 2D migration assay after 48 h in culture (n = 5). HANP/GKT831 reduced the protein levels of representative signal molecules in glycolysis, mitochondrial OXPHOS, and DNA repair pathways. C. The levels of Western blot analysis of NOX1, NOX4, glycolysis related (Hexokinase 2 and PKM2), and mitochondrial OXPHOS associated proteins (MT-ATP6 and MT-ND1). D. The protein levels in the cell cycle and DNA repair pathway, Cyclin D1, MSH6, and CHK1 proteins, were examined from the treated tumor lysates by Western blot analysis. β-actin served as the loading control. Similar results were obtained from at least 3 repeated studies. Student’s t-test: *p < 0.05 and ****p < 0.0001.

    Article Snippet: After transferring to a polyvinylidene difluoride and blocking in 5 % of milk in tris-buffered saline (TBS) for 1 h, the blots were probed with rabbit anti-NOX1 antibody (MBS9609001, MYBioSource, San Diego, CA, USA), rabbit anti-NOX4 antibody (MBS820230, MYBioSource), anti-Hexokinase II rabbit monoclonal antibody (C64G5, Cell Signaling Technology), anti PKM2 XP rabbit monoclonal antibody (D78A4, Cell Signaling Technology), rabbit anti-MT-ATP6 antibody (70262, Cell Signaling Technology), rabbit anti-MT-ND1 antibody (NBP2-94462, NOVUS, MO, USA), anti-Cyclin D1 rabbit monoclonal antibody (2978, Cell Signaling Technology), rabbit anti-MSH6 antibody (MBS9626584, MYBioSource), rabbit anti-Phospho-Chk1 (Ser345) antibody (#2341, Cell Signaling Technology), hamster anti MCP-1 (CCL2) antibody (505911, Biolegend, San Diego, CA, USA), rabbit antiCXCL10 monoclonal antibody (701225, Invitrogen), anti-β-Actin mouse monoclonal antibody (A5316, Sigma-Aldrich).

    Techniques: Migration, Colony Assay, Transwell Migration Assay, Western Blot, Control