NDUFB6 (Human) Recombinant Protein (P01)

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NDUFB6 (Human) Recombinant Protein (P01) Catalog # : H00004712-P01 規格 : [ 10 ug ] [ 25 ug ] List All Specification Application Image Product Human NDUFB6 full-length ORF ( AAH29247, 1 a.a. - 128 a.a.) Enzyme-linked Immunoabsorbent Assay Description: recombinant protein with GST-tag at N-terminal. Western Blot (Recombinant Sequence: MTGYTPDEKLRLQQLRELRRRWLKDQELSPREPVLPPQKMGPMEKFW protein) NKFLENKSPWRKMVHGVYKKSIFVFTHVLVPVWIIHYYMKYHVSEKPYGIV EKKSRIFPGDTILETGEVIPPMKEFPDQHH Antibody Production Host: Wheat Germ (in vitro) Protein Array Theoretical MW 39.82 (kDa): Preparation in vitro wheat germ expression system Method: Purification: Glutathione Sepharose 4 Fast Flow Quality Control 12.5% SDS-PAGE Stained with Coomassie Blue. Testing: Storage Buffer: 50 mM Tris-HCI, 10 mM reduced Glutathione, pH=8.0 in the elution buffer. Storage Store at -80°C. Aliquot to avoid repeated freezing and thawing. Instruction: Note: Best use within three months from the date of receipt of this protein. MSDS: Download Datasheet: Download Applications Enzyme-linked Immunoabsorbent Assay Western Blot (Recombinant protein) Antibody Production Page 1 of 2 2016/5/21 Protein Array Gene Information Entrez GeneID: 4712 GeneBank BC029247 Accession#: Protein AAH29247 Accession#: Gene Name: NDUFB6 Gene Alias: B17,CI,MGC13675 Gene NADH dehydrogenase (ubiquinone) 1 beta subcomplex, 6, 17kDa Description: Omim ID: 603322 Gene Ontology: Hyperlink Gene Summary: The protein encoded by this gene is a subunit of the multisubunit NADH:ubiquinone oxidoreductase (complex I). Mammalian complex I is composed of 45 different subunits. It locates at the mitochondrial inner membrane. This protein has NADH dehydrogenase activity and oxidoreductase activity. It transfers electrons from NADH to the respiratory chain. The immediate electron acceptor for the enzyme is believed to be ubiquinone. Alternative splicing occurs at this locus and two transcript variants encoding distinct isoforms have been identified. [provided by RefSeq Other NADH dehydrogenase (ubiquinone) 1 beta subcomplex, 6 (17kD, Designations: B17),NADH-ubiquinone oxidoreductase B17 subunit,NADH-ubiquinone oxidoreductase beta subunit, 6,OTTHUMP00000021179,OTTHUMP00000021180,complex I, mitochondrial respiratory chain, B17 subunit Gene Pathway Alzheimer's disease Huntington's disease Metabolic pathways Oxidative phosphorylation Parkinson's disease Related Disease Diabetes Mellitus, Type 2 Genetic Predisposition to Disease Prostatic Neoplasms 服務條款 | 隱私權政策 | 著作及商標 | 網站地圖 ©2016 亞諾法生技股份有限公司 Abnova Corporation. 版權所有. Page 2 of 2 2016/5/21.

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The Pathogenetic Role of Β-Cell Mitochondria in Type 2 Diabetes
236 3 Journal of M Fex et al. Mitochondria in β-cells 236:3 R145–R159 Endocrinology REVIEW The pathogenetic role of β-cell mitochondria in type 2 diabetes Malin Fex1, Lisa M Nicholas1, Neelanjan Vishnu1, Anya Medina1, Vladimir V Sharoyko1, David G Nicholls1, Peter Spégel1,2 and Hindrik Mulder1 1Department of Clinical Sciences in Malmö, Unit of Molecular Metabolism, Lund University Diabetes Centre, Clinical Research Center, Malmö University Hospital, Lund University, Malmö, Sweden 2Department of Chemistry, Center for Analysis and Synthesis, Lund University, Sweden Correspondence should be addressed to H Mulder: [email protected] Abstract Mitochondrial metabolism is a major determinant of insulin secretion from pancreatic Key Words β-cells. Type 2 diabetes evolves when β-cells fail to release appropriate amounts f TCA cycle of insulin in response to glucose. This results in hyperglycemia and metabolic f coupling signal dysregulation. Evidence has recently been mounting that mitochondrial dysfunction f oxidative phosphorylation plays an important role in these processes. Monogenic dysfunction of mitochondria is a f mitochondrial transcription rare condition but causes a type 2 diabetes-like syndrome owing to β-cell failure. Here, f genetic variation we describe novel advances in research on mitochondrial dysfunction in the β-cell in type 2 diabetes, with a focus on human studies. Relevant studies in animal and cell models of the disease are described. Transcriptional and translational regulation in mitochondria are particularly emphasized. The role of metabolic enzymes and pathways and their impact on β-cell function in type 2 diabetes pathophysiology are discussed. The role of genetic variation in mitochondrial function leading to type 2 diabetes is highlighted.
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