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PDP - Template Name: Antibody Sampler Kit
PDP - Template ID: *******4a3ef3a

Electron Transport Chain (Complex I, III, IV) Antibody Sampler Kit #42642

    Product Information

    Product Description

    The Electron Transport Chain (Complex I, III, IV) Antibody Sampler Kit provides an economical means of detecting select components involved in the electron transport chain (ETC) (Complex I, III, IV). The kit includes enough antibodies to perform two western blot experiments with each primary antibody.

    Specificity / Sensitivity

    Each antibody in the Electron Transport Chain (Complex I, III, IV) Antibody Sampler Kit detects endogenous levels of its target protein. COX1/MT-CO1 (E2I2R) Rabbit mAb does not cross-react with COX2/MT-CO2 protein or COX3/MT-CO3 protein.

    Source / Purification

    Monoclonal antibodies are produced by immunizing animals synthetic peptides corresponding to residues surrounding Ile286 of human NDUFS1 protein, Pro72 of human cytochrome c protein, Lys29 of human COX IV protein, Asp31 of human COX10 protein, and near the carboxy terminus of human ACP/NDUFAB1 protein and human COX1/MT-CO1 protein.

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro86 of human UQCRFS1/RISP protein. Antibodies are purified by peptide affinity chromatography.

    Background

    Mitochondrial acyl carrier protein (ACP) is an essential component in fatty acid biosynthesis in mitochondria. It is also known as NADH-ubiquinone oxidoreductase subunit AB1 (NDUFAB1), a Complex I subunit in the electron transport chain (ETC). NDUFAB1 regulates energy and reactive oxygen species (ROS) metabolism in mitochondria by coordinating the assembly of ETC Complexes I, II, and III, and supercomplexes (1). NDUFS1 (NADH dehydrogenase Fe-S protein 1) is a nuclear-encoded structural subunit of NADH: ubiquinone oxidoreductase (Complex I) in the mitochondrial ETC (2). Mutations in NDUFS1 and other Complex I subunits leading to mitochondrial dysfunction are associated with a number of neurological disorders (3-6). Ubiquinol-cytochrome c reductase iron-sulfur subunit (UQCRFS1), also known as Rieske iron-sulfur protein (RISP), is a component of Complex III in the mitochondrial ETC. UQCRFS1/RISP and two other subunits, cytochrome b (MT-CYB) and cytochrome c1 (CYC1), are essential for the catalytic activity of Complex III (7). Cytochrome c is a well conserved electron transport protein and is part of the respiratory chain localized to mitochondrial intermembrane space (8). Upon apoptotic stimulation, cytochrome c released from mitochondria associates with procaspase-9 (47 kDa)/Apaf-1. This complex processes caspase-9 from inactive proenzyme to its active form (9). This event further triggers caspase-3 activation and eventually leads to apoptosis (10). The mitochondrial ETC comprises multiple protein complexes, including cytochrome c oxidase. Cytochrome c oxidase catalyzes the reduction of oxygen to water. This process is coupled with pumping protons from the mitochondrial matrix into mitochondrial intermembrane space, contributing to the proton gradient used for ATP synthesis (11). Cytochrome c oxidase consists of 3 mitochondrial DNA-encoded subunits (COX1/MT-CO1, COX2/MT-CO2, and COX3/MT-CO3) and multiple nuclear DNA-encoded subunits (12). Research studies show that the mRNAs of the mitochondrially encoded oxidative phosphorylation subunits, including COX1/MT-CO1, decline significantly during aging (13). Cytochrome c oxidase (COX, also known as Complex IV) is a hetero-oligomeric enzyme consisting of 13 subunits localized to the inner mitochondrial membrane (14-16). It is the terminal enzyme complex in the respiratory chain, catalyzing the reduction of molecular oxygen to water coupled to the translocation of protons across the mitochondrial inner membrane to drive ATP synthesis. The 3 largest subunits forming the catalytic core are encoded by mitochondrial DNA, while the other smaller subunits, including COX IV, are nuclear-encoded. Research studies have shown that deficiency in COX activity correlates with a number of human diseases (17). COX10 is an assembly factor for cytochrome c oxidase in the mitochondrial ETC (18,19). Studies show that, when the gene encoding the β2-adrenergic receptor (Adrb2) is deleted, increased oxidative phosphorylation in endothelial cells inhibits angiogenesis. Deletion of Cox10 prevents the metabolic switch to oxidative phosphorylation in endothelial cells deleted of Adrb2, causing angiogenesis and cancer progression (19). In addition, COX10 contributes to T cell quiescence exit and is critical for T cell activation (20).
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    19. Zahalka, A.H. et al. (2017) Science 358, 321-326.
    20. Tan, H. et al. (2017) Immunity 46, 488-503.
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