Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.6.5.3 (complex I)
 8,901 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The 20.9 kDa subunit of NADH:ubiquinone oxidoreductase (complex I) from Neurospora crassa is a nuclear-coded component of the hydrophobic arm of the enzyme. We have determined the primary structure of this subunit by sequencing a full-length cDNA and a cleavage product of the isolated polypeptide. The deduced protein sequence is 189 amino acid residues long and contains a putative membrane-spanning domain. Striking similarity over a 60 amino-acid-residue domain with the M (matrix) protein of para-influenza virus was found. No other relationship with already known sequences could be detected, leaving the function of this subunit in complex I still undefined. The biogenetic pathway of this polypeptide was studied using a mitochondrial import system in vitro. The 20.9 kDa subunit synthesized in vitro is efficiently imported into isolated mitochondria, where it obtains distinct features of the endogenous subunit. Our results suggest that the 20.9 kDa polypeptide is made on cytosolic ribosomes lacking a cleavable targeting sequence, interacts with the mitochondrial outer membrane (in a process that does not require an energized inner membrane), and is imported into mitochondria at contact sites. The 20.9 kDa subunit is then inserted into the inner membrane acquiring a topology similar to that of the already assembled subunit.
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PMID:Primary structure and mitochondrial import in vitro of the 20.9 kDa subunit of complex I from Neurospora crassa. 144 73

(CBA X C57B1) X F1 mice were sensitized intraperitoneally with sheep erythrocytes and infected with influenza A viruses: nonpathogenic Leningrad-77 (H1N1) or pathogenic PR8 (HON1), before or five days after administration into the oesophagus of sodium succinate, levamisole, complexes I (panangin, sodium succinate, sodium glutamate) and 2 (lipoic acid, phosphothyamine, riboflavin, sodium pantothenate). The number of rosette-forming cells (RFC) in the spleen at 7 and 14 days postinfection, antibody titres, interferon level in the blood, the amount of virus in the lungs, spleen and lung morphology were studied. All the preparations used were found to increase the number of RFC in the spleen. Most effective were levamisole before infection, sodium succinate after infection, combination thereof, complex I after infection.
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PMID:[Effect of a number of preparations on the function of the immune system in experimental influenza in mice]. 651 25

We report on a 4-year-old boy who died from influenza encephalopathy. The clinical course and microscopic findings of the autopsied liver were compatible with Reye's syndrome. We examined the mitochondrial respiratory chain function by blue native polyacrylamide gel electrophoresis (BN-PAGE), western blotting, and respiratory chain enzyme activity assays. The activity of liver respiratory chain complex (CO) I was markedly decreased (7.2% of the respective control activity); whereas, the other respiratory chain complex activities were substantially normal (CO II, 57.9%; CO III, 122.3%; CO IV, 161.0%). The activities of CO I-IV in fibroblasts were normal (CO I, 82.0%; CO II, 83.1%; CO III, 72.9%; CO IV, 97.3%). The patient was diagnosed with liver-specific complex I deficiency. This inborn disorder may have contributed to the fatal outcome. We propose that relying only on fibroblast respiratory chain complex activities may lead to the misdiagnosis of liver-specific complex I deficiency.
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PMID:Liver-specific mitochondrial respiratory chain complex I deficiency in fatal influenza encephalopathy. 2144 Oct 7