EC Number   |
General Information |
Reference |
|---|
   3.4.21.79 | evolution |
the identification of a granzyme B homologue with aspase (cleaving after aspartic acid) specificity in a non-placental mammal provides strong indications that caspase or Bid-dependent apoptosis by a serine protease with a conserved primary specificity has been part of anti-viral immunity since early mammalian evolution. An asp-ase together with a chymase were the first two serine protease genes to appear in the mammalian chymase locus. The mast cell chymase and GzmB were the first two enzymes to appear in this locus. Granzyme B is the only member of the hematopoietic serine proteases, which cleaves after negatively charged amino acids. Phylogenetic analysis and tree, overview |
755124 |
| 3.4.21.79 | malfunction |
increased circulating granzyme B in type 2 diabetes patients with low-grade systemic inflammation, correlated with unfavorable inflammatory profile, as described by elevated levels of validated adipokines such as interleukin-6, TNF-alpha, and WISP1. Multivariate linear regression analysis shows that increased GrB is associated with type 2 diabetes diagnosis independently from possible confounders |
753362 |
| 3.4.21.79 | malfunction |
inhibition of granzyme B activity blocks inflammation induced by lipopolysaccharide through regulation of endoplasmic reticulum stress signaling in NK92 cells. Inhibition of GrB activity suppresses the changes of NF-kappaB and IkappaBalpha expression levels induced by LPS as part of endoplasmic reticulum stress |
754761 |
| 3.4.21.79 | malfunction |
inhibition or downregulation of GrB suppresses bladder cancer cell invasion in vitro |
708765 |
| 3.4.21.79 | malfunction |
knockout GzmB-/- mice which have a small deletion in the granzyme B gene express granzyme C earlier and more abundantly in lymphocytes on a per-cell basis compared to wild-type, suggesting that the deleted 350-bp region in the granzyme B gene is important for the regulation of both granzymes B and granzyme C. Intraepithelial lymphocytes in GzmB-/- knockout mice likewise express granzyme C |
709346 |
| 3.4.21.79 | malfunction |
the mouse pathogen Brucella microti persists in mice lacking perforin or granzyme B as well as in mice depleted of Tc cells |
-, 731617 |
| 3.4.21.79 | malfunction |
Tresp cells from patients with multiple sclerosis resist Treg suppression via a mechanism that involves GzmB |
732275 |
| 3.4.21.79 | metabolism |
gzmB+ cytotoxic T cell-mediated apoptosis (via phosphatidylserine translocation, mitochondrial depolarization, cytochrome c release, and caspase-3 activation) is severely reduced in 3T9 cells lacking either Bim or both Bak and Bax, gzmB+ cytotoxic T cell-mediated apoptosis is not affected in SV40-transformed mouse embryonic fibroblast cells lacking Bak/Bax.Role of Bim in gzmB-mediated apoptosis, overview |
-, 732185 |
| 3.4.21.79 | more |
effects of GrB cleavage on the structure, processing, and immunogenicity of PAD4, overview |
754488 |
| 3.4.21.79 | more |
establishment of an enzymatic assay to detect and quantify the expression of functional granzyme B protein. Using this assay, the levels of killing of different Theileria parva-specific CD8+ T-cell clones are found to be significantly correlated with the levels of granzyme B protein but not the levels of mRNA transcript expression. Using inhibitors specific for perforin and granzyme B confirms that CD8+ T-cell killing of parasitized cells is dependent on granule exocytosis and, specifically, granzyme B |
-, 753808 |
