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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. Additionally we are shipping Mitochondrially Encoded NADH Dehydrogenase 5 Kits (12) and Mitochondrially Encoded NADH Dehydrogenase 5 Proteins (4) and many more products for this protein.
Showing 10 out of 59 products:
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 (show COX2 Antibodies) 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 (show COX2 Antibodies) (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 (show COX2 Antibodies) = cytochrome c oxidase subunit II (show COX2 Antibodies))
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 (show TBRG4 Antibodies) is required to promote expression of ND5. FASTKD4 (show TBRG4 Antibodies) may promote processing of ND5-CYB (show CSTB Antibodies) 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 (show NDUFA1 Antibodies) subunit, complex I extracts energy from NADH, produced by the oxidation of sugars and fats (show C10ORF90 Antibodies), and traps the energy in a potential difference or voltage across the mitochondrial inner membrane.
Study demonstrates a link between p53 (show TP53 Antibodies) and Bcl-2 (show BCL2 Antibodies) proteins as regulators of ROS (show ROS1 Antibodies) 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 (show MT-ND4 Antibodies) and MT-ND5 genes.
Point mutations m.10191T>C in mitochondrial ND3 (show MT-ND3 Antibodies) gene, m.13513G>A in ND5 gene and m.14,453G>A in ND6 (show MT-ND6 Antibodies) 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 (show EGFR Antibodies) 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