Human NDUFS1 ELISA Kit (V2LY-0626-LY5647)

Name: Human NDUFS1 ELISA Kit
SKU: V2LY-0626-LY5647
Rating: 5 (1 reviews)

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Tested Data

Datasheet

SDS

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Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Sensitivity

0.011 ng/mL

Detection Range

0.02-3.8 ng/mL

Sample Type

Serum, Plasma, cell culture supernates

Specificity

Human

Assay Type

Sandwich

Reactivity

Human

Assay Time

1.5 h

Molecule Mass

79.5 kDa

Components

Pre-coated ELISA plate: 12 wells * 8 detachable strips
Standard solution: 0.5ml x1
Standard diluent: 3ml x1
Streptavidin-HRP: 6ml x1
Stop solution: 6ml x1
Substrate solution A: 6ml x1
Substrate solution B: 6ml x1
Wash buffer concentrate (25x): 20ml x1
Biotinylated antibody: 1ml x1

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

Storage

Store at 2-8°C

More Infomation

Target

Full Name

NADH:ubiquinone oxidoreductase core subunit S1

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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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme Linked Immunospot (ELISpot)
Proteogenomic
Other Protocols

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Isotype control

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

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We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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