EC Number   |
General Information |
Reference |
|---|
   3.4.21.78 | evolution |
the enzyme belongs to the granzyme serine protease family, key effector molecules expressed by cytotoxic lymphocytes. Peptide substrate specificity profile of mouse and human granzyme A, overview |
732177 |
| 3.4.21.78 | malfunction |
even though granzyme A is expressed by cytotoxic cells from mouse lungs during pulmonary infection, its deficiency in knockout mice does not have an effect in the control of Mycobacterium tuberculosis infection |
-, 755118 |
| 3.4.21.78 | malfunction |
phenotypic characterization of gzmA-/- regulatory T cells (Tregs) efficiently homing to secondary lymphoid organs, GzmA-/- Tregs home efficiently to secondary lymphoid organs, overview. No difference between wild-type and GZMA-/- mice in Treg numbers in spleen and peripheral lymph nodes. Enzyme-deficient gzmA-/- Tregs cannot efficiently protect from GvHD-related inflammation and organ destruction in the intestinal tract with relevant crypt apoptosis detected in the small and large intestine |
755083 |
| 3.4.21.78 | malfunction |
pneumonia is induced in wild-type and GzmA-deficient (GzmA-/-) mice by intranasal inoculation of Streptococcus pneumoniae. In separate experiments, wild-type and GzmA-/- mice are treated with natural killer (NK) cell depleting antibodies. Upon infection, GzmA-/- mice show a better survival and lower bacterial counts in bronchoalveolar lavage fluid (BALF) and distant body sites compared to the wild-type mice. Although NK cells show strong GzmA expression, NK cell depletion does not influence bacterial loads in either wild-type or GzmA-/- mice. GzmA deficiency has little impact on lung pathology during late stage pneumococcal pneumonia |
-, 752445 |
| 3.4.21.78 | metabolism |
CD8 T cells in psoriasis skinlesions display a dominant expression of granzyme A (GzmA) over granzyme B in the absence of perforin expression. Signals recruiting GzmA+ T cells into the skin and triggers of GzmA expression in the context of chronic inflammation, Tc17-polarizing conditions favour development of GzmA+GzmB-Prf-CD8 T-cells in the context of psoriasis |
753512 |
| 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 |
