Literature summary for 3.4.21.B2 extracted from

Anthony, D.A.; Andrews, D.M.; Chow, M.; Watt, S.V.; House, C.; Akira, S.; Bird, P.I.; Trapani, J.A.; Smyth, M.J.
A role for granzyme M in TLR4-driven inflammation and endotoxicosis (2010), J. Immunol., 185, 1794-1803.

Search for more literature for 3.4.21.B2

Cloned(Commentary)

Cloned (Comment)	Organism
recombinant GrzM produced from Pichia pastoris	Mus musculus

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	-	wild-type C57BL/6 mice and B6 RAG12/2 gene-targeted mice	-

Synonyms

Synonyms	Comment	Organism
Granzyme M	-	Mus musculus
GrzM	-	Mus musculus

Expression

Organism	Comment	Expression
Mus musculus	GrzM is exclusively expressed by natural killer cells	up

General Information

General Information	Comment	Organism
malfunction	a lack of GrzM results in reduced serum IL-1alpha, IL-1beta, TNF, and IFN-gamma levels and significantly reduces susceptibility to lipopolysaccharide-induced lethal endotoxicosis	Mus musculus
physiological function	is a potential key regulator of inflammation: natural killer cell GrzM augments the inflammatory cascade downstream of lipopolysaccharide-TLR4 signaling, which ultimately results in lethal endotoxicosis. Caspase-1 is upstream of GrzM in the lipopolysaccharide model of sepsis. Lipopolysaccharide-driven natural killer cell IFN-gamma production is caspase-1 dependent and regulated by GrzM	Mus musculus

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Release 2023.1 (January 2023)