Anti-MGME1 Mouse Mab

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Anti-MGME1 Mouse mAb Catalog # PTM-5474 General Information Images Host species Mouse WB Clonality Recombinant monoclonal Blocking buffer: 5% NFDM/TBST Clone number JMMR-1656 Primary ab dilution: 1:1000 Synonym C20orf72, DDK1 Primary ab incubation condition: 4°C overnight Immunogen UniProt MW (kDa) Applications Secondary ab: Goat Anti-Mouse IgG H&L species (HRP) Human Q9BQP7 39 WB Lysate: HeLa, HepG2, A549 Protein loading quantity: 20 μg Product Usage Information Exposure time: 60 s Predicted MW: 39 kDa Application Dilution Recommended species Observed MW: 35 kDa WB 1:500-1:1000 Human Research Use Properties For research use only, not for use in diagnostic procedures. Storage Store at -20°C. Avoid freeze / thaw cycles. Stability Stable for 12 months from date of receipt / reconstitution Constituents PBS, Glycerol, BSA Purity Protein G purified Isotype IgG1/Kappa Target Information Function Metal-dependent single-stranded DNA (ssDNA) exonuclease involved in mitochondrial genome maintenance. Has preference for 5'-3' exonuclease activity but is also capable of endoduclease activity on linear substrates. Necessary for maintenance of proper 7S DNA levels. Probably involved in mitochondrial DNA (mtDNA) repair, possibly via the processing of displaced DNA containing Okazaki fragments during RNA-primed DNA synthesis on the lagging strand or via processing of DNA flaps during long-patch base excision repair. Specifically binds 5-hydroxymethylcytosine (5hmC)- containing DNA in stem cells. Cellular location Mitochondrion APPLICATIONS WB: Western blot IP: Immunoprecipitation CONTACT US China Global IHC-P: Immunohistochemistry-Paraffin ChIP: Chromatin Immunoprecipitation Tel: 400-100-1145 +1 312-802-6843 ICC/IF: Immunocytochemistry/Immunofluorescence FC: Flow Cytometry Email: [email protected] [email protected] Web: www.ptm-biolab.com.cn www.ptmbiolabs.com .

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Mice Lacking the Mitochondrial Exonuclease MGME1 Accumulate Mtdna Deletions Without Developing Progeria
ARTICLE DOI: 10.1038/s41467-018-03552-x OPEN Mice lacking the mitochondrial exonuclease MGME1 accumulate mtDNA deletions without developing progeria Stanka Matic1, Min Jiang1, Thomas J. Nicholls2, Jay P. Uhler2, Caren Dirksen-Schwanenland1, Paola Loguercio Polosa3, Marie-Lune Simard1, Xinping Li4, Ilian Atanassov 4, Oliver Rackham 5, Aleksandra Filipovska5, James B. Stewart 1, Maria Falkenberg2, Nils-Göran Larsson 1,6 & Dusanka Milenkovic 1 1234567890():,; Replication of mammalian mitochondrial DNA (mtDNA) is an essential process that requires high fidelity and control at multiple levels to ensure proper mitochondrial function. Mutations in the mitochondrial genome maintenance exonuclease 1 (MGME1) gene were recently reported in mitochondrial disease patients. Here, to study disease pathophysiology, we generated Mgme1 knockout mice and report that homozygous knockouts develop depletion and multiple deletions of mtDNA. The mtDNA replication stalling phenotypes vary drama- tically in different tissues of Mgme1 knockout mice. Mice with MGME1 deficiency accumulate a long linear subgenomic mtDNA species, similar to the one found in mtDNA mutator mice, but do not develop progeria. This finding resolves a long-standing debate by showing that point mutations of mtDNA are the main cause of progeria in mtDNA mutator mice. We also propose a role for MGME1 in the regulation of replication and transcription termination at the end of the control region of mtDNA. 1 Department of Mitochondrial Biology, Max Planck Institute for Biology of Ageing, Cologne 50931, Germany. 2 Department of Medical Biochemistry and Cell Biology, University of Gothenburg, Gothenburg 405 30, Sweden. 3 Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari Aldo Moro, Bari 70125, Italy.
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