Gene: ATP5MC3
Official Full Name: ATP synthase membrane subunit c locus 3provided by HGNC
Gene Summary: This gene encodes a subunit of mitochondrial ATP synthase. Mitochondrial ATP synthase catalyzes ATP synthesis, utilizing an electrochemical gradient of protons across the inner membrane during oxidative phosphorylation. ATP synthase is composed of two linked multi-subunit complexes: the soluble catalytic core, F1, and the membrane-spanning component, Fo, comprising the proton channel. The catalytic portion of mitochondrial ATP synthase consists of 5 different subunits (alpha, beta, gamma, delta, and epsilon) assembled with a stoichiometry of 3 alpha, 3 beta, and a single representative of the other 3. The proton channel seems to have nine subunits (a, b, c, d, e, f, g, F6 and 8). This gene is one of three genes that encode subunit c of the proton channel. Each of the three genes have distinct mitochondrial import sequences but encode the identical mature protein. Alternatively spliced transcript variants encoding different proteins have been identified. [provided by RefSeq, Jun 2010]
Catalog Number | Product Name | Species | Gene | Passage ratio | Mycoplasma testing | Price |
---|---|---|---|---|---|---|
KO05552 | ATP5MC3 Knockout cell line (HeLa) | Human | ATP5MC3 | 1:3~1:6 | Negative | Online Inquiry |
KO05553 | ATP5MC3 Knockout cell line (HCT 116) | Human | ATP5MC3 | 1:2~1:4 | Negative | Online Inquiry |
KO05554 | ATP5MC3 Knockout cell line (HEK293) | Human | ATP5MC3 | 1:3~1:6 | Negative | Online Inquiry |
KO05555 | ATP5MC3 Knockout cell line (A549) | Human | ATP5MC3 | 1:3~1:4 | Negative | Online Inquiry |
ATP5MC3 Gene Knockout Cell Lines are specialized cell models designed to facilitate the study of mitochondrial function and cellular energy metabolism by eliminating the ATP5MC3 gene, which is crucial for encoding a subunit of the mitochondrial ATP synthase complex. The targeted knockout of this gene disrupts the formation and stability of the ATP synthase enzyme, which plays a pivotal role in ATP production through oxidative phosphorylation. This unique alteration offers researchers a powerful tool to investigate the downstream effects of impaired mitochondrial function and energy production at both the cellular and organismal levels.
The primary mechanism of ATP5MC3 gene knockout involves CRISPR-Cas9 technology, allowing for precise and efficient genome editing. By introducing double-strand breaks at specific locations within the ATP5MC3 locus, researchers can generate knockout cell lines that provide deeper insights into pathways associated with cellular metabolism, apoptosis, and diseases linked to mitochondrial dysfunction such as neurodegenerative disorders, diabetes, and certain types of cancer.
The scientific importance of these cell lines lies in their versatility, enabling applications across both research and clinical settings. They serve as invaluable models for drug development, mitochondrial disease research, and the testing of therapeutic strategies aimed at mitigating the effects of mitochondrial impairments. By studying these knockout cell lines, researchers can screen for novel compounds that target energy metabolism and elucidate the role of mitochondrial dysfunction in various pathologies.
Compared to other genetic models, ATP5MC3 gene knockout cell lines offer distinct advantages, including high fidelity in gene editing, reproducible results, and the ability to be cultured under standardized conditions. This enhances the reliability of experimental outcomes and accelerates research timelines. Researchers, clinicians, and pharmaceutical developers can therefore leverage these models to discover new therapeutic targets and validate potential treatments more effectively.
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