granzyme B

This is an abbreviated version!
For detailed information about granzyme B, go to the full flat file.

Word Map on EC


preferential cleavage: -Asp-/- >> -Asn-/- > -Met-/-, -Ser-/- =


CTLA1, CCPII, Cytotoxic cell proteinase-1, Granzyme G, Granzyme H, Proteinase, CCP1, HLp, C11, CCP1, CTSGL1, Human lymphocyte protein, Lymphocyte protease, SECT, T-cell serine protease 1-3E, GrB, rat grB[N66Q], natural killer cell protease 1, pro-apoptotic serine protease, cytotoxic T-lymphocyte-associated gene transcript-1, GzmB, GzmH, GzB, GrzmB, cytotoxic lymphocyte-associated protease, cytotoxic lymphocyte-specific protein, gB, cytotoxic serine protease granzyme B, granzyme B, proGrB, Gzm, Gzm B, Gra-b, Asp-ase, GzmB-like enzyme


     3 Hydrolases
         3.4 Acting on peptide bonds (peptidases)
             3.4.21 Serine endopeptidases
       granzyme B


Expression on EC - granzyme B

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enzyme expression is decreased in natural killer cells following immunosuppressive therapy
expression of granzyme B is higher in patients with Bronchiolitis obliterans syndrome than in patients with acute lung transplant rejection
expression of GrB mRNA is upregulated in active lesions of multiple sclerosis patients and in activated T cells
extracellular levels of the ezyme are elevated in the bodily fluids in chronic inflammatory diseases such as atherosclerosis and rheumatoid arthritis
GrB expression in plasmacytoid dendritic cells is strictly regulated on a transcriptional level involving Janus kinase 1 (JAK1), signal transducer and activator of transcription 3 (STAT3), and STAT5. Interleukin-3 (IL-3), secreted by activated T cells, plays a central role for GrB induction
GrB in urothelial cancer tissues is concentrated at the cancer invasion front and is expressed in neoplastic cells undergoing epithelial-mesenchymal transition, a key event in carcinoma invasion
IL-21 directly induces GzmB expression and secretion by CD51 B cells
in blood, bronchoalveolar lavage (BAL) and large airway brushing expression of granzyme B is significantly increased in lung transplant patients
increased circulating granzyme B in type 2 diabetes patients with low-grade systemic inflammation
interleukin-6 induces CD4 T cells to express the enzyme
regulatory T cells (Tregs) freshly isolated from the peripheral blood of normal adults lack granzyme B expression. Tregs subjected to prolonged TCR and CD28 triggering, in the presence of IL-2, express high levels of granzyme B but CD3 stimulation alone or IL-2 treatment alone fail to induce granzyme B
serine protease inhibitor A3N, i.e. serpin A3N or SA3N, an extracellular inhibitor of GrB possessing multiple biological functions, including the attenuaxadtion of muscular dystrophy in mice, neuropathic pain, and GrB-mediated decorin cleavage and rupture. It also induces neuroprotection in vitro and in vivo. Role of GrB inhibitor SA3N on Escherichia coli LPS-induced inflammation in NK-92 cells. SA3N pretreatment prevents the LPS-induced changes in expression levels of GRP78, CHOP, NF-kappaB and IkappaBalpha proteins. Also SA3N pretreatment prevents the expression and exocytosis of GrB by LPS
serum levels of GrB are elevated in several diseases such as human immunodeficiency virus-1 infection, Epstein-Barr virus infection, arthritis and others
stimulation of NK cells in vitro with IL-15 induce expression of granzyme C
treatment of regulatory T cells (Tregs) with the mammalian target of rapamycin (mTOR) inhibitor, rapamycin or the PI3 kinase (PI3K) inhibitor LY294002 markedly suppresses granzyme B expression