Literature summary for 1.15.1.1 extracted from

Call, J.A.; Donet, J.; Martin, K.S.; Sharma, A.K.; Chen, X.; Zhang, J.; Cai, J.; Galarreta, C.A.; Okutsu, M.; Du, Z.; Lira, V.A.; Zhang, M.; Mehrad, B.; Annex, B.H.; Klibanov, A.L.; Bowler, R.P.; Laubach, V.E.; Peirce, S.M.; Yan, Z.
Muscle-derived extracellular superoxide dismutase inhibits endothelial activation and protects against multiple organ dysfunction syndrome in mice (2017), Free Radic. Biol. Med., 113, 212-223 .

Cloned(Commentary)

Cloned (Comment)	Organism
recombinant expression in Mus musculus, CX3CR1-GFP mice, heterogenic parabiosis between mutant and wild-type mice confers a significant protection to wild-type mice, whereas mice with R213G knock-in mutation, a human single nucleotide polymorphism leading to reduced binding EcSOD in peripheral organs, exacerbate the organ damages. Recombinant EcSOD overexpressed in skeletal muscle-specific mutant mice redistributes to other peripheral organs through the circulation and enriches at the endothelium of the vasculatures. Mutant mice are resistant to endotoxemia (induced by lipopolysaccharide injection) in developing MODS with significantly reduces mortality and organ damages compared with the wild-type littermates	Mus musculus

Cloned (Comment)

Organism

recombinant expression in Mus musculus, CX3CR1-GFP mice, heterogenic parabiosis between mutant and wild-type mice confers a significant protection to wild-type mice, whereas mice with R213G knock-in mutation, a human single nucleotide polymorphism leading to reduced binding EcSOD in peripheral organs, exacerbate the organ damages. Recombinant EcSOD overexpressed in skeletal muscle-specific mutant mice redistributes to other peripheral organs through the circulation and enriches at the endothelium of the vasculatures. Mutant mice are resistant to endotoxemia (induced by lipopolysaccharide injection) in developing MODS with significantly reduces mortality and organ damages compared with the wild-type littermates

Mus musculus

Protein Variants

Protein Variants	Comment	Organism
R213G	site-directed mutagenesis, mutant mice with R213G knock-in mutation, a human single nucleotide polymorphism leading to reduced binding EcSOD in peripheral organs, exacerbate the organ damages. Phenotype, overview	Mus musculus

Localization

Localization	Comment	Organism	GeneOntology No.	Textmining
extracellular	-	Mus musculus	-	-

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	-	-	-
Mus musculus C57BL/6J	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
skeletal muscle	muscle-derived extracellular superoxide dismutase	Mus musculus	-

Synonyms

Synonyms	Comment	Organism
ECSOD	-	Mus musculus
extracellular superoxide dismutase	-	Mus musculus

General Information

General Information	Comment	Organism
malfunction	enhanced EcSOD expression in skeletal muscle inhibits endothelial activation, EcSOD is sufficient to inhibit endothelial activation in vitro and in vivo	Mus musculus
physiological function	EcSOD inhibits vascular cell adhesion molecule 1 expression and inflammatory leukocyte adhesion to the vascular wall of vital organs, blocking an early step of the pathology in organ damage under endotoxemia. Enhanced expression of EcSOD in skeletal muscle profoundly protects against Multiple organ dysfunction syndrome (MODS) by inhibiting endothelial activation and inflammatory cell adhesion, which might be a promising therapy for MODS	Mus musculus