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Rabbit Anti-NDUFS1 Recombinant Antibody (CBWJN-0966) (CBMAB-N0214-WJ)

This product is a Rabbit antibody that recognizes NDUFS1. The antibody CBWJN-0966 can be used for immunoassay techniques such as: WB, IP, IHC-P, FC, ICC.
See all NDUFS1 antibodies

Summary

Host Animal
Rabbit
Specificity
Mouse, Rat, Human
Clone
CBWJN-0966
Antibody Isotype
IgG
Application
WB, IP, IHC-P, FC, ICC

Basic Information

Specificity
Mouse, Rat, Human
Antibody Isotype
IgG
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
NADH:ubiquinone oxidoreductase core subunit S1
Introduction
The protein encoded by this gene belongs to the complex I 75 kDa subunit family. Mammalian complex I is composed of 45 different subunits. It locates at the mitochondrial inner membrane. This protein has NADH dehydrogenase activity and oxidoreductase activity. It transfers electrons from NADH to the respiratory chain. The immediate electron acceptor for the enzyme is believed to be ubiquinone. This protein is the largest subunit of complex I and it is a component of the iron-sulfur (IP) fragment of the enzyme. It may form part of the active site crevice where NADH is oxidized. Mutations in this gene are associated with complex I deficiency. Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jan 2011]
Entrez Gene ID
Human4719
Mouse227197
Rat301458
UniProt ID
HumanP28331
MouseQ91VD9
RatQ66HF1
Alternative Names
NADH:Ubiquinone Oxidoreductase Core Subunit S1; NADH Dehydrogenase (Ubiquinone) Fe-S Protein 1, 75kDa (NADH-Coenzyme Q Reductase); NADH-Ubiquinone Oxidoreductase 75 KDa Subunit, Mitochondrial; Complex I 75kDa Subunit; CI-75Kd; NADH Dehydrogenase (Ubiquinone) Fe-S Protein 1 (75kD) (NADH-Coenzyme Q Reductase); Mitochondrial NADH-Ubiquinone Oxidoreductase 75 KDa Subunit;
Function
Core subunit of the mitochondrial membrane respiratory chain NADH dehydrogenase (Complex I) which catalyzes electron transfer from NADH through the respiratory chain, using ubiquinone as an electron acceptor (PubMed:30879903, PubMed:31557978).

Essential for catalysing the entry and efficient transfer of electrons within complex I (PubMed:31557978).

Plays a key role in the assembly and stability of complex I and participates in the association of complex I with ubiquinol-cytochrome reductase complex (Complex III) to form supercomplexes (PubMed:30879903, PubMed:31557978).
Biological Process
Aerobic respiration Source: ComplexPortal
Apoptotic mitochondrial changes Source: UniProtKB
ATP metabolic process Source: UniProtKB
Cellular respiration Source: UniProtKB
Mitochondrial ATP synthesis coupled proton transport Source: ComplexPortal
Mitochondrial electron transport, NADH to ubiquinone Source: UniProtKB
Mitochondrial respiratory chain complex I assembly Source: UniProtKB
Reactive oxygen species metabolic process Source: UniProtKB
Regulation of mitochondrial membrane potential Source: UniProtKB
Cellular Location
Mitochondrion inner membrane
Involvement in disease
Mitochondrial complex I deficiency, nuclear type 5 (MC1DN5):
A form of mitochondrial complex I deficiency, the most common biochemical signature of mitochondrial disorders, a group of highly heterogeneous conditions characterized by defective oxidative phosphorylation, which collectively affects 1 in 5-10000 live births. Clinical disorders have variable severity, ranging from lethal neonatal disease to adult-onset neurodegenerative disorders. Phenotypes include macrocephaly with progressive leukodystrophy, non-specific encephalopathy, cardiomyopathy, myopathy, liver disease, Leigh syndrome, Leber hereditary optic neuropathy, and some forms of Parkinson disease. MC1DN5 transmission pattern is consistent with autosomal recessive inheritance.

Ren, L., Meng, L., Gao, J., Lu, M., Guo, C., Li, Y., ... & Ye, Y. (2023). PHB2 promotes colorectal cancer cell proliferation and tumorigenesis through NDUFS1-mediated oxidative phosphorylation. Cell Death & Disease, 14(1), 44.

Chen, T., Li, D., Wang, Y., Shen, X., Dong, A., Dong, C., ... & Zhou, J. (2023). Loss of NDUFS1 promotes gastric cancer progression by activating the mitochondrial ROS-HIF1α-FBLN5 signaling pathway. British Journal of Cancer, 129(8), 1261-1273.

Wu, D., He, L., Xu, Z., Tian, R. F., Fan, X. Y., Fan, J., ... & Li, L. (2023). The combination of NDUFS1 with CD4+ T cell infiltration predicts favorable prognosis in kidney renal clear cell carcinoma. Frontiers in Cell and Developmental Biology, 11.

Qi, B., Song, L., Hu, L., Guo, D., Ren, G., Peng, T., ... & Li, Y. (2022). Cardiac-specific overexpression of Ndufs1 ameliorates cardiac dysfunction after myocardial infarction by alleviating mitochondrial dysfunction and apoptosis. Experimental & Molecular Medicine, 54(7), 946-960.

Zou, R., Tao, J., Qiu, J., Shi, W., Zou, M., Chen, W., ... & Chen, X. (2021). Ndufs1 deficiency aggravates the mitochondrial membrane potential dysfunction in pressure overload-induced myocardial hypertrophy. Oxidative Medicine and Cellular Longevity, 2021.

Qi, B., He, L., Zhao, Y., Zhang, L., He, Y., Li, J., ... & Ji, L. (2020). Akap1 deficiency exacerbates diabetic cardiomyopathy in mice by NDUFS1-mediated mitochondrial dysfunction and apoptosis. Diabetologia, 63, 1072-1087.

Elkholi, R., Abraham-Enachescu, I., Trotta, A. P., Rubio-Patiño, C., Mohammed, J. N., Luna-Vargas, M. P., ... & Chipuk, J. E. (2019). MDM2 integrates cellular respiration and apoptotic signaling through NDUFS1 and the mitochondrial network. Molecular cell, 74(3), 452-465.

Ni, Y., Hagras, M. A., Konstantopoulou, V., Mayr, J. A., Stuchebrukhov, A. A., & Meierhofer, D. (2019). Mutations in NDUFS1 cause metabolic reprogramming and disruption of the electron transfer. Cells, 8(10), 1149.

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For research use only. Not intended for any clinical use.

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