3.4.21.B2: granzyme M
This is an abbreviated version!
For detailed information about granzyme M, go to the full flat file.
Word Map on EC 3.4.21.B2
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3.4.21.B2
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lymphocyte
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granule
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killer
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perforin
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medicine
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cell-mediated
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virus-infected
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cytolysis
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pore-forming
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caspase-independent
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thiobenzyl
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serpins
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perforin-dependent
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m-mediated
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norleucine
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noncytotoxic
- 3.4.21.B2
- lymphocyte
- granule
-
killer
- perforin
- medicine
-
cell-mediated
-
virus-infected
-
cytolysis
-
pore-forming
-
caspase-independent
-
thiobenzyl
- serpins
-
perforin-dependent
-
m-mediated
- norleucine
-
noncytotoxic
Reaction
endopeptidase activity. Cleaves substrates containing a methionine side chain at P1 =
Synonyms
Granzyme M, GrM, GrzM, Gzm M, GZmM, hGzmM, hMet-1, Met-ase-1, S01.139
ECTree
3.4.21.B2 granzyme MAdvanced search results
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General Information on EC 3.4.21.B2 - granzyme M
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GENERAL INFORMATION 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
malfunction
physiological function
malfunction
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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
malfunction
in absence of granzyme M colonic inflammation is enhanced. The absence of granzyme expression also has effects on gut permeability, tissue cytokine/chemokine dynamics, and neutrophil infiltration during disease
physiological function
Gzm M shows apoptotic activity both by caspase dependent and independent pathways
physiological function
GzmM associates with survivin. Survivin cleavage by GzmM abolishes the stability of the survivin-X-linked inhibitor of apoptosis protein complex and enhances X-linked inhibitor of apoptosis protein hydrolysis, which amplifies caspase-9 and 3 activation of target tumor cells
physiological function
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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
physiological function
granzyme M induced cell death is largely caspase-dependent with various hallmarks of classical apoptosis, coinciding with caspase-independent G2/M cell cycle arrest. The nuclear enzyme topoisomerase II alpha is a physiological substrate of granzyme M. Cleavage of topoisomerase II alpha by granzyme M at Leu1280 separates topoisomerase II alpha functional domains from the nuclear localization signals, leading to nuclear exit of topoisomerase II alpha catalytic activity, thereby rendering it nonfunctional. Similar to the apoptotic phenotype of granzyme M, topoisomerase II alpha depletion in tumor cells leads to cell cycle arrest in G2/M, mitochondrial perturbations, caspase activation, and apoptosis
physiological function
granzyme M induces the epithelial mesenchymal transition in cancer cells associated with STAT3 activation. It increases chemoresistance, colony formation, cytokine secretion and invasiveness
physiological function
granzyme M induces the epithelial mesenchymal transition in cancer cells associated with STAT3 activation. It increases chemoresistance, colony formation, cytokine secretion and invasiveness
physiological function
the enzyme has a critical role in providing innate immune protection in ulcerative colitis. It has a critical role during early stages of inflammation in ulcerative colitis
physiological function
the enzyme is involved in killing of tumor cells and virally infected cells. It contributes to cytokine release and processing
