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GZMK product is a member of a group of related serine proteases from the cytoplasmic granules of cytotoxic lymphocytes. Additionally we are shipping Granzyme K (Granzyme 3, Tryptase II) Antibodies (86) and Granzyme K (Granzyme 3, Tryptase II) Kits (32) and many more products for this protein.
Showing 10 out of 14 products:
these data suggest that granzyme K does not play an essential role in viral immunity or cytotoxicity
The data suggest that T-killer cells control lymphocytic choriomeningitis virus through non-cytotoxic processes that involve gzmK.
It was suggested that a high predisposition to catalepsy in mice can be defined by the Map3k1 (show MAP3K1 Proteins), Il6st, Gzmk, and Hspb3 (show HSPB3 Proteins) genes' coexpression network.
GzmK-induced caspase (show CASP3 Proteins)-independent death occurs through Bid (show BID Proteins)-dependent mitochondrial damage that is different from GzmA (show GZMA Proteins)
grzK plays an important role in CD8 (show CD8A Proteins)(+) T-cell cytotoxicity both in the presence and absence of grzA and B.
Extracellular granzyme K mediates endothelial activation through the cleavage of PAR-1 (show MARK2 Proteins).
Carbamate pesticides significantly reduced the intracellular levels of perforin (show PRF1 Proteins), GrA (show NR3C1 Proteins), GrB, Gr3 (show PRLHR Proteins)/K, and GRN (show GRN Proteins) in NK-92CI cells.
Extracellular GrK (show GRK4 Proteins) is an unexpected direct modulator of lipopolysaccharide-TLR4 (show TLR4 Proteins) signaling during the antimicrobial innate immune response.
Granzyme K plays an important physiological role in immunoregulation of adaptive immunity underlying the cytotoxicity of CD56 (show NCAM1 Proteins)(bright) natural killer (NK) cells toward activated T cells.
Gr3 (show PRLHR Proteins) proenzymes is activated by cathepsin C (show CTSC Proteins) which concomitantly decreased the molecular weight to that of active Gr3 (show PRLHR Proteins).
The present findings thus introduce the possibility that human beta-tryptase (show TPSAB1 Proteins), after mast cell degranulation and exposure to neutral pH in the tissue, may dissociate into active monomers with properties that are distinct from the tetrameric counterpart.
We found human GzmK triggers rapid cell death independently of caspase (show CASP3 Proteins) activation. The features of death are characterized by rapid externalization of phosphatidylserine, nuclear morphological changes and single-stranded DNA nicks.
Rsults indicate that plasma levels of Granzyme K could serve as a useful diagnostic marker to stage sepsis, permitting better classification, specific treatments of patients, and may play a functional role in the development of sepsis.
GrK (show GRK4 Proteins) not only constitutes a redundant functional backup mechanism that assists GrA (show NR3C1 Proteins)-induced cell death but that it also displays a unique function by cleaving its own specific substrates.
Data show that the serum levels of mast cell tryptase, monocyte chemoattractant protein-1 (MCP-1 (show CCL2 Proteins)) and interleukin-8 (IL-8 (show IL8 Proteins)) decreased significantly in Dachengqi decoction treatment group.
This gene product is a member of a group of related serine proteases from the cytoplasmic granules of cytotoxic lymphocytes. Cytolytic T lymphocytes (CTL) and natural killer (NK) cells share the remarkable ability to recognize, bind, and lyse specific target cells. They are thought to protect their host by lysing cells bearing on their surface 'nonself' antigens, usually peptides or proteins resulting from infection by intracellular pathogens. The protein described here lacks consensus sequences for N-glycosylation present in other granzymes.
, granzyme 3
, granzyme K
, granzyme K (serine protease, granzyme 3; tryptase II)
, tryptase II