NADH Dehydrogenase (Ubiquinone) Fe-S Protein 1, 75kDa (NADH-Coenzyme Q Reductase) Proteins (NDUFS1)

Mouse (Murine) NADH Dehydrogenase (Ubiquinone) Fe-S Protein 1, 75kDa (NADH-Coenzyme Q Reductase) (NDUFS1) interaction partners

1. lysosomal membrane permeability induced by TNFalpha (show TNF Proteins) plus cycloheximide, the release of lysosomal cathepsins and reactive oxygen species formation require the caspase-3 (show CASP3 Proteins)-mediated cleavage of the p75 (show NGFR Proteins) NDUFS1 subunit of respiratory complex I.

Human NADH Dehydrogenase (Ubiquinone) Fe-S Protein 1, 75kDa (NADH-Coenzyme Q Reductase) (NDUFS1) interaction partners

1. Results show that NDUFS1 protein and mRNA levels are down-regulated in lung neoplasm and correlate with poor overall survival.

2. High NDUFS1 expression is associated with cognitive impairment in lung cancer.

3. Results found nominal significant associations of 2 SNPs in the NDUFS1 gene and 4 SNPs in the NDUFS2 (show NDUFS2 Proteins) gene with early onset schizophrenia (EOS (show IKZF4 Proteins)), but none of these associations survived the Bonferroni correction.

4. Loss of FOXRED1 (show FOXRED1 Proteins), coupled with protein, choline and/or folate-deficient diets results in the depletion of glutathione, the dysregulation of nitric oxide metabolism and the peroxynitrite-mediated inactivation of complex I.

5. NDUFS1 may confer susceptibility to schizophrenia in male subjects, acting as a causative factor for the severity of negative symptoms in schizophrenia.

6. The presented clinical courses of NDUFV1 (show NDUFV1 Proteins) and NDUFS1 mutation-based complex I deficiencies are characterized by leukoencephalopathy or early death and expand the already heterogeneous phenotypic spectrum.

7. Some mutations in NDUFS1 cause a milder phenotype with a more benign course despite the initial decompensation phase. Homozygosity for the c.755A > G missense mutation may correlate with the milder clinical picture in the patient.

8. homozygous c.1783A>G (p.Thr595Ala) mutation in NDUFS1 in two inbred siblings with isolated complex I deficiency associated to a progressive cavitating leukoencephalopathy

9. report 3 patients with low residual complex I activity who displayed novel mutations in the NDUFS1 gene. One mutation introduces a premature stop codon, 3 mutations cause a substitution of amino acids and another mutation a deletion of one amino acid.

10. A patient with Leigh syndrome had a mutation in the NDUFS1 protein of Complex I of the Respiratory Chain. Identifying nuclear mutations will help us understand how molecular defects can lead to complex I deficiency.

Cow (Bovine) NADH Dehydrogenase (Ubiquinone) Fe-S Protein 1, 75kDa (NADH-Coenzyme Q Reductase) (NDUFS1) interaction partners

1. Data show that during NADH-ubiquinone oxidoreductase (Complex (show NDUFA2 Proteins) I) catalytic electron transfer from NADH to DBQ, the superoxide generation site was mostly shifted to the SQ.

2. Data suggest that Q(Nf) plays a role in a "direct" redox-driven proton pump, while Q(Ns) triggers an "indirect" conformation-driven proton pump in NADH-ubiquinone oxidoreductase (complex (show NDUFA2 Proteins) I).

3. Bovine heart NADH-ubiquinone oxidoreductase contains one molecule of ubiquinone with ten isoprene units as one of the cofactors