Literature summary for 7.1.1.1 extracted from

Rao, K.; Shen, X.; Pardue, S.; Krzywanski, D.
Nicotinamide nucleotide transhydrogenase (NNT) regulates mitochondrial ROS and endothelial dysfunction in response to angiotensin II (2020), Redox Biol., 36, 101650 .

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Localization

Localization	Comment	Organism	GeneOntology No.	Textmining
mitochondrion	-	Homo sapiens	5739	-

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	Q13423	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
endothelial cell	-	Homo sapiens	-

General Information

General Information	Comment	Organism
physiological function	NNT expression and activity are elevated in response to the mitochondrial dysfunction and oxidative stress associated with angiotensin II treatment. Knockdown of NNT leads to a significant elevation of mitochondrial ROS production and impaired glutathione peroxidase and glutathione reductase activities associated with a reduction in the NADPH/NADP+ ratio. Loss of NNT also promotes mitochondrial dysfunction, disruption of the mitochondrial membrane potential, and impaired ATP production in response to angiotensin II. The loss of NNT augments endothelial nitric oxide synthase phosphorylation at Ser1177, but neither endothelial nitric oxide synthase activity nor nitric oxide production are similarly increased	Homo sapiens

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Release 2023.1 (January 2023)