Abcam, ab263104, Human ATP5G3 knockout HEK-293T cell lysate

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ATP5MC3 KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, Homozygous: 11 bp deletion in exon 3.
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: 11 bp deletion in exon 3.

Product details:
Knockout cell lysate achieved by CRISPR/Cas9.
REACH authorisation
Abcam has not and does not intend to apply for the REACH Authorisation of customers' uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.
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
patent pages

Properties and Storage Information:
Gene name-ATP5MC3, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Zygosity-Homozygous, Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
ATP5G3 also known as ATP synthase F0 subunit C3 or mitochondrial ATP synthase membrane subunit C locus 3 is a component of the ATP synthase complex. This protein has an approximate mass of 8.2 kDa. It is expressed in many tissues with high levels observed in metabolically active organs such as the heart liver and skeletal muscle. The primary role of ATP5G3 involves contributing to the formation of the proton channel in the mitochondrial membrane which is essential for ATP synthesis during cellular respiration.
Biological function summary
ATP5G3 plays an important role in the mitochondrial ATP synthase complex also referred to as Complex V part of the electron transport chain. This complex catalyzes the conversion of ADP and inorganic phosphate into ATP using the proton gradient established by the complexes I-IV. ATP5G3 through its mechanical function helps maintain the efficiency of ATP production within cells. Its operation is important for cellular energy supply supporting processes like muscle contraction and biosynthetic reactions.
Pathways
ATP5G3 integrates into the oxidative phosphorylation pathway where it interacts with other subunits of the ATP synthase complex to ensure ATP synthesis. This pathway coordinates with the citric acid cycle (Krebs cycle) which generates the electrons used to establish the proton gradient necessary for ATP production. Proteins such as cytochrome c and NADH dehydrogenase (Complex I) connect with ATP5G3 through their roles in the electron transport chain creating a streamlined flow of electron transfer and energy conversion.
Dysregulation of ATP5G3 can contribute to conditions like mitochondrial myopathy and Leigh syndrome where impaired ATP synthesis leads to reduced cellular energy output. Mitochondrial dysfunctions with ATP5G3 at the center often relate to oxidative stress and metabolic imbalances. Connections with cytochrome c and other electron transport components illustrate the broader impact of ATP5G3 disruptions leading to the progression of these diseases through compromised cellular respiration and energy homeostasis.