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Literature summary for 7.1.1.1 extracted from

  • Sharaf, M.S.; Stevens, D.; Kamunde, C.
    Mitochondrial transition ROS spike (mTRS) results from coordinated activities of complex I and nicotinamide nucleotide transhydrogenase (2017), Biochim. Biophys. Acta, 1858, 955-965 .
    View publication on PubMed
Search for more literature for 7.1.1.1

Localization

Localization Comment Organism GeneOntology No. Textmining
mitochondrion
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 Oncorhynchus mykiss 5739
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Organism

Organism UniProt Comment Textmining
Oncorhynchus mykiss A0A060X964
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-

Source Tissue

Source Tissue Comment Organism Textmining
heart
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 Oncorhynchus mykiss
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liver
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 Oncorhynchus mykiss
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Synonyms

Synonyms Comment Organism
nicotinamide nucleotide transhydrogenase
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 Oncorhynchus mykiss

General Information

General Information Comment Organism
physiological function pharmacological inhibition of complex CI, nicotinamide nucleotide transhydrogenase NNT and antioxidant system significantly decreases the ability of mitochondria to exhibit mitochondrial transition ROS spike (mTRS). NADH levels follow a similar trend to that of ROS during the mTRS. mTRS is enhanced by simultaneous activation of CI and complex II and NNT regulates mTRS via NADH- and membrane potential-dependent mechanisms. mTRS changes in amplitude under stress conditions and its occurrence can be a signature of mitochondrial health Oncorhynchus mykiss