Gene: NDUFA10
Official Full Name: NADH:ubiquinone oxidoreductase subunit A10provided by HGNC
Gene Summary: The protein encoded by this gene is a component of 42 kDa complex I, the first enzyme complex in the electron transport chain of mitochondria. This protein has NADH dehydrogenase activity and oxidoreductase activity. It transfers electrons from NADH to the respiratory chain. A mutation in this gene was found in an individual with Leigh syndrome. [provided by RefSeq, Apr 2016]
Catalog Number | Product Name | Species | Gene | Passage ratio | Mycoplasma testing | Price |
---|---|---|---|---|---|---|
KO36439 | NDUFA10 Knockout cell line (HeLa) | Human | NDUFA10 | 1:3~1:6 | Negative | Online Inquiry |
KO36440 | NDUFA10 Knockout cell line (HCT 116) | Human | NDUFA10 | 1:2~1:4 | Negative | Online Inquiry |
KO36441 | NDUFA10 Knockout cell line (HEK293) | Human | NDUFA10 | 1:3~1:6 | Negative | Online Inquiry |
KO36442 | NDUFA10 Knockout cell line (A549) | Human | NDUFA10 | 1:3~1:4 | Negative | Online Inquiry |
NDUFA10 Gene Knockout Cell Lines are genetically engineered cell lines that specifically target and disrupt the NDUFA10 gene, a crucial component of the mitochondrial electron transport chain. This gene encodes a subunit of the NADH:ubiquinone oxidoreductase complex, also known as Complex I, which plays a vital role in ATP production through oxidative phosphorylation. By employing CRISPR/Cas9 technology, NDUFA10 knockout cell lines allow researchers to study the implications of NDUFA10 deficiency on cellular metabolism, mitochondrial function, and overall energy homeostasis.
The primary function of these knockout cell lines is to provide a controlled environment for investigating the effects of diminished Complex I activity. When NDUFA10 is inactivated, researchers can better understand the resultant metabolic shifts—such as alterations in glycolysis and the tricarboxylic acid cycle—as well as the activation of compensatory pathways. These models are indispensable for elucidating disease mechanisms associated with mitochondrial dysfunction, including neurodegenerative disorders, metabolic syndromes, and cardiomyopathies, thereby paving the way for the development of targeted therapies.
One distinct advantage of these NDUFA10 gene knockout cell lines is their precision in replicating physiological conditions under which the NDUFA10 gene is absent. This specificity addresses limitations commonly found in pharmacological inhibitors or other genetic knockdown techniques, which may produce off-target effects. Consequently, researchers can derive more reliable data, advancing their understanding of mitochondrial diseases.
Given their robust functionality and targeted approach, NDUFA10 knockout cell lines are invaluable to both academic and clinical research. They offer significant insights into the metabolic consequences of NDUFA10 deletion, aiding in the exploration of novel therapeutic interventions aimed at restoring mitochondrial health.
Our company's expertise in cellular engineering ensures that these knockout cell lines are not only rigorously validated but also developed with stringent quality standards to meet the diverse needs of researchers and clinicians. By integrating cutting-edge genetic modification techniques with comprehensive support services, we provide a unique offering that enhances the quality and efficiency of scientific inquiry in mitochondrial research.
Please note that all services are for research use only. Not intended for any clinical use.
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