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Literature summary for 1.1.1.284 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
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Cloned(Commentary)

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

Protein Variants

Protein Variants Comment Organism
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

Localization Comment Organism GeneOntology No. Textmining
mitochondrion
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 Sus scrofa 5739
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Organism

Organism UniProt Comment Textmining
Sus scrofa F1S0C1
-
-

Source Tissue

Source Tissue Comment Organism Textmining
blastocyst
-
 Sus scrofa
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embryo
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 Sus scrofa
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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
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Synonyms

Synonyms Comment Organism
S-nitrosoglutathione reductase
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 Sus scrofa

General Information

General Information Comment Organism
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
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