EC Number   |
General Information  |
Reference |
|---|
   3.4.21.78 | physiological function |
granzyme A contributes to the early inflammatory response in the lung. Granzyme A (GzmA) impairs host defense during Streptococcus pneumoniae pneumonia, role of GzmA on the host response during pneumococcal pneumonia, overview |
752445 |
| 3.4.21.78 | physiological function |
granzyme A contributes to the early inflammatory response in the lung. Granzyme A (GzmA) plays an unfavorable role in host defense during pneumococcal pneumonia by a mechanism that does not depend on natural killer cells. GzmA enhances bacterial dissemination and mortality in pneumococcal pneumonia |
-, 752445 |
| 3.4.21.78 | physiological function |
granzyme A from cytotoxic lymphocytes cleaves gasdermin B to trigger pyroptosis in target cells. This immune effector mechanism promotes cytotoxic T lymphocyte-mediated tumor clearance in mice |
776005 |
| 3.4.21.78 | physiological function |
granzyme A is expressed in mouse lungs during Mycobacterium tuberculosis strain H37Rv infection but does not contribute to protection in vivo. Granzyme A does not have a crucial role in vivo in the protective response to tuberculosis |
-, 755118 |
| 3.4.21.78 | physiological function |
granzyme A is required for regulatory T-cell mediated prevention of gastrointestinal graft-versus-host disease. Analysis of the role of granzyme A (GZMA) in a haploidentical murine graft-versus-host disease (GvHD) model using gzmA-/- donor regulatory T cells (Tregs) to clarify the functional relevance of GZMA for Treg-mediated suppression of GvHD. GZMA expressing Tregs protect against GvHD-related tissue damage of the intestine |
755083 |
| 3.4.21.78 | physiological function |
high functional activity of GzmA in the innate cell-mediated cytotoxicity |
771416 |
| 3.4.21.78 | physiological function |
histone H4 is cleaved by granzyme A during staurosporine-induced cell death in B-lymphoid Raji cells. A fast-migrating histone H4 fragment is detected in cells undergoing staurosporine-induced cell death. Treatment with caspase inhibitors (inhibitors of caspase-6 (Z-VEID-FMK) and caspase-9 (Z-LEHD-FMK)) increases both cell death and histone H4 cleavage. The enzyme cleaves the N-terminal tail pf H4. The cleavage of the histone H4 tail by GzmA contributes to the disintegration of chromosomes during the cell death process. The SET complex is normally located in the endoplasmic reticulum, but it translocates to the nucleus in response to reactive oxygen species produced by GzmA-mediated cleavage of NADH dehydrogenase (ubiquinone) Fe-S protein 3. GzmA is mobilized in the nucleus where many of its known substrates reside. In the nucleus, GzmA digests three components of the SET complex: SET, high-mobility group protein B2, and apurinic/apyrimidinic endonuclease. SET is an inhibitor of the SET complex endonuclease NM23-H1. GzmA degrades the linker histone H1 and removes the tails from core histones H2 and H3, opening up the chromatin and making it accessible to nucleases |
753077 |
| 3.4.21.78 | physiological function |
in filarial infection with Litomosoides sigmodontis, worm loads are significantly reduced in gzmA/gzmB and in gzmB knockout mice during the whole course of infection, but enhanced only early in gzmA knockout compared with wild-type mice. GzmA/gzmB deficiency is associated with a defense-promoting Th2 cytokine and Ab shift, enhanced early inflammatory gene expression, and a trend of reduced alternatively activated macrophage induction, whereas gzmA deficiency is linked with reduced inflammation and a trend toward increased alternatively activated macrophages |
717939 |
| 3.4.21.78 | physiological function |
interleukin-17 induced secretion of the cytokines interleukin-6, interleukin-8 and interleukin-23, whereas GzmA treatment alone does not induce secretion of inflammatory mediators. The combination of GzmA and interleukin-17 significantly increases the release of the proinflammatory chemokines CXCL 1, CXCL 12, and CCL 4 compared to interleukin-17 stimulation alone, but does not alter the levels of interleukin-17-induced cytokines interleukin-6, interleukin-8 and interleukin-23. GzmA neither promotes proliferation nor affects interleukin-17-induced keratinocyte differentiation status as measured by gene expression of MKI67, IVL, KRT16 or KRT10 |
753512 |
| 3.4.21.78 | physiological function |
recombinant GrA promotes release of interleukin IL-8 from A-549 cells, without involvement of protease-activated receptor-1. Release is inhibited by taxol |
708274 |
