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Core subunit of the mitochondrial membrane respiratory chain NADH dehydrogenase (Complex I) that is believed to belong to the minimal assembly required for catalysis. 再加上，我们可以发Mitochondrially Encoded NADH Dehydrogenase 5 试剂盒 (12) 和 Mitochondrially Encoded NADH Dehydrogenase 5 蛋白 (4)和数多这个蛋白质的别的产品。
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Human Polyclonal MT-ND5 Primary Antibody for IF (p), IHC (p) - ABIN751633
Wu, Zhang, Nickerson, Gao, Sun, Chen, Zhang, Zhang, Gao, Chen, Luo, Wang, Sun: Cumulative mtDNA damage and mutations contribute to the progressive loss of RGCs in a rat model of glaucoma. in Neurobiology of disease 2015
Data suggest that mutations in MT-CO2 (显示 COX2 抗体) and MT-ND5 can be involved in MIDD (maternally inherited diabetes and deafness); a Tunisian family (mother, daughter, son) with clinical features of MIDD associated with retinopathy exhibit mutations in MT-CO2 (显示 COX2 抗体) (m.8241T>G - p. F219C) and MT-ND5 (m.13276G>A - p. M314V); these two mutations could explain retinopathy in some family members. (MT-CO2 (显示 COX2 抗体) = cytochrome c oxidase subunit II (显示 COX2 抗体))
A MELAS/Leigh syndrome phenotype caused by a mtDNA mutation [m.13513G>A; p.Asp393Asn] in the ND5 gene encoding the ND5 subunit of respiratory chain complex I was identified in a patient in a second family
FASTKD4 (显示 TBRG4 抗体) is required to promote expression of ND5. FASTKD4 (显示 TBRG4 抗体) may promote processing of ND5-CYB (显示 CSTB 抗体) precursor or it may stabilize multiple mature RNAs including ND5.
The m.13565C>T mutation in MTND5 causes defects in both mitochondrial oxidative metabolism and mitochondrial calcium sequestration in a MELAS syndrome fibroblasts.
Mitochondrially encoded NADH dehydrogenase (显示 NDUFA1 抗体) subunit, complex I extracts energy from NADH, produced by the oxidation of sugars and fats (显示 C10ORF90 抗体), and traps the energy in a potential difference or voltage across the mitochondrial inner membrane.
Study demonstrates a link between p53 (显示 TP53 抗体) and Bcl-2 (显示 BCL2 抗体) proteins as regulators of ROS (显示 ROS1 抗体) production and cellular invasiveness, and reveals complex-I, especially ND5, as their functional target in lung tumor cells.
Three mutations were significantly related to the presence of epilepsy. These mutations were found at the 8502, 11994, and 13,231 bp of mtDNA, which resulted in amino acid changes at the MT-ATP-8, MT-ND4 (显示 MT-ND4 抗体) and MT-ND5 genes.
Point mutations m.10191T>C in mitochondrial ND3 (显示 MT-ND3 抗体) gene, m.13513G>A in ND5 gene and m.14,453G>A in ND6 (显示 MT-ND6 抗体) gene were detected in three Chinese children with Leigh synrome dur to complex I deficiency.
Mitochondrial ND5 12338T>C variant is associated with maternally inherited hypertrophic cardiomyopathy in a Chinese pedigree
Mitochondrial DNA mutations in respiratory complex-I in never-smoker lung cancer patients contribute to lung cancer progression in association with EGFR (显示 EGFR 抗体) gene mutation.
Core subunit of the mitochondrial membrane respiratory chain NADH dehydrogenase (Complex I) that is believed to belong to the minimal assembly required for catalysis. Complex I functions in the transfer of electrons from NADH to the respiratory chain. The immediate electron acceptor for the enzyme is believed to be ubiquinone (By similarity).
NADH dehydrogenase subunit 5