Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary extracted from

  • Niu, Y.J.; Zhou, D.; Cui, X.S.
    S-nitrosoglutathione reductase maintains mitochondrial homeostasis by promoting clearance of damaged mitochondria in porcine preimplantation embryos (2021), Cell Prolif., 54, e12990 .
    View publication on PubMedView publication on EuropePMC

Cloned(Commentary)

EC Number Cloned (Comment) Organism
1.1.1.284 gene ADH5, quantitative reverse transcription PCR enzyme expression analysis Sus scrofa

Protein Variants

EC Number Protein Variants Comment Organism
1.1.1.284 additional information GSNOR dsRNA is employed to knockdown the expression of GSNO. GSNOR knock-down induces oxidative stress-derived apoptosis and DNA damage, as well as inhibits autophagic process Sus scrofa

Localization

EC Number Localization Comment Organism GeneOntology No. Textmining
1.1.1.284 mitochondrion
-
 Sus scrofa 5739
-

Organism

EC Number Organism UniProt Comment Textmining
1.1.1.284 Sus scrofa F1S0C1
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
1.1.1.284 blastocyst
-
 Sus scrofa
-
1.1.1.284 embryo
-
 Sus scrofa
-
1.1.1.284 additional information GSNOR protein is expressed at all stages during porcine preimplantation embryo development in both cytoplasmic and nuclear of preimplantation embryos, but gradually reduced during embryo development Sus scrofa
-

Synonyms

EC Number Synonyms Comment Organism
1.1.1.284 S-nitrosoglutathione reductase
-
 Sus scrofa

General Information

EC Number General Information Comment Organism
1.1.1.284 malfunction GSNOR knockdown significantly impairs blastocyst formation and quality and markedly induces the increase in protein S-nitrosylation. Notably, GSNOR knockdown-induced overproduction of S-nitrosylation caused mitochondrial dysfunction, including mitochondrial membrane potential depolarization, mitochondria-derived reactive oxygen species (ROS) increase and ATP deficiency. GSNOR knockdown-induced total mitochondrial amount increase, but the ratio of active mitochondria reduction, suggesting that the damaged mitochondria are accumulated and mitochondrial clearance is inhibited. In addition, damaged mitochondria produce more ROS, and cause DNA damage and apoptosis. Supplementation with pan-NOS inhibitor Nomega-nitro-L-arginine methyl ester hydrochloride (L-NAME) reverses the increase in S-nitrosylation, accumulation of damaged mitochondria, and oxidative stress-induced cell death. Autophagy is downregulated after GSNOR knock-down, but reversed by L-NAME treatment Sus scrofa
1.1.1.284 physiological function S-nitrosoglutathione reductase maintains mitochondrial homeostasis by promoting clearance of damaged mitochondria in porcine preimplantation embryos. GSNOR maintains mitochondrial homeostasis by promoting autophagy and the clearing of damaged mitochondria in porcine preimplantation embryos Sus scrofa