Literature summary for 3.1.4.3 extracted from

Tumurkhuu, G.; Koide, N.; Dagvadorj, J.; Noman, A.S.; Iftekar-E-Khuda, I.; Naiki, Y.; Komatsu, T.; Yoshida, T.; Oda, M.; Nagahama, M.; Sakurai, J.; Yokochi, T.
The inhibition of lipopolysaccharide-induced tumor necrosis factor-alpha and nitric oxide production by Clostridium perfringens alpha-toxin and its relation to alpha-toxin-induced intracellular ceramide generation (2009), Int. J. Med. Microbiol., 299, 554-562.

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Protein Variants

Protein Variants	Comment	Organism
H148G	pretreatment of the inactive mutant H148G losing PLC and SMase activities does not affect the production of NO and tumor necrosis factor-alpha in lipopolysaccharide-stimulated RAW264.7 cells	Clostridium perfringens

Organism

Organism	UniProt	Comment	Textmining
Clostridium perfringens	-	-	-

Purification (Commentary)

Purification (Comment)	Organism
wild-type and mutant H148G	Clostridium perfringens

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
p-nitrophenylphosphoryl-choline + H2O	-	Clostridium perfringens	p-nitrophenol + phosphorylcholine	-	?

Synonyms

Synonyms	Comment	Organism
alpha-toxin	-	Clostridium perfringens

General Information

General Information	Comment	Organism
physiological function	alpha-toxin inhibits the expression of tumor necrosis factor-alpha and an inducible type of NO synthase protein and mRNA. It inhibits the phosphorylation of IkappaB-alpha and p65 NF-kappaB subunit, and the NF-kappaB luciferase reporter gene activity in lipopolysaccharide-stimulated RAW 264.7 cells. Pretreatment of alpha-toxin increases the level of intracellular ceramide. Treatment with alpha-toxin alone leads to the phosphorylation of mitogen-activated protein kinases	Clostridium perfringens

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Release 2023.1 (January 2023)