NDUFA7 KO cell lysate available now. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, Homozygous: 8 bp deletion in exon 1.
B14.5a, CI-B14.5a, Complex I-B14.5a, NADH dehydrogenase (ubiquinone) 1 alpha subcomplex 7 14.5kDa, NADH dehydrogenase [ubiquinone] 1 alpha subcomplex subunit 7, NADH-ubiquinone oxidoreductase subunit B14.5a, NDUA7_HUMAN
NDUFA7 KO cell lysate available now. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, Homozygous: 8 bp deletion in exon 1.
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Lysate preparation: Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10). This means that the protein of interest is denatured. If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.
User storage instructions: Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.
This product is subject to limited use licenses from The Broad Institute and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our limited use license and patent pages.
The NDUFA7 protein also known as NADH dehydrogenase [ubiquinone] 1 alpha subcomplex subunit 7 is an integral part of the mitochondrial respiratory chain. It has a molecular weight of approximately 12 kDa. This protein is expressed mostly in the mitochondria of various cells and tissues such as muscle liver and brain. It plays a significant role in the electron transport chain where it contributes to the transfer of electrons from NADH to ubiquinone therefore contributing to ATP production.
The NDUFA7 protein operates as a component of the mitochondrial complex I also referred to as NADH:ubiquinone oxidoreductase. This complex which includes around 45 different subunits is the first and largest enzyme of the mitochondrial respiratory chain. NDUFA7 does not directly catalyze the electron transfer but stabilizes the structure of the complex necessary for efficient electron flow. Proper functioning of complex I is essential for maintaining cellular energy homeostasis and normal metabolic activity.
NDUFA7 plays an important role within the oxidative phosphorylation pathway which is important for aerobic energy production. This protein is closely related to other proteins in complex I such as NDUFA9 which together ensure efficient functioning of the electron transfer process. Moreover NDUFA7 indirectly influences other metabolic networks that rely on ATP including the TCA cycle and fatty acid oxidation highlighting its fundamental contribution to cellular metabolism.
Mutations in the NDUFA7 gene can lead to mitochondrial disorders such as Leigh syndrome and mitochondrial complex I deficiency. These are serious conditions that may result in motor disability developmental challenges and other systemic problems. In the context of these disorders NDUFA7 interacts with proteins like NDUFS1 which also constitutes a part of complex I and defects in these proteins can amplify mitochondrial dysfunction highlighting the interconnectedness of protein actions within the cell.
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Homozygous: 8 bp deletion in exon 1
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