EC Number   |
Natural Substrates   |
|---|
 3.4.21.78 | protein NDUFS3 + H2O |
GzmA cleavage of native Ndufs3 disrupts complex I electron transport |
 3.4.21.78 | NADH dehydrogenase (ubiquinone) Fe-S protein 3 + H2O |
- |
 3.4.21.78 | more |
cell death-inducing serine protease |
 3.4.21.78 | more |
most abundant protease in cytotoxic T lymphocytes, granzyme A pathway of cell-mediated cytotoxicity, produced as proenzyme, activated by the dipetidyl exopeptidase cathepsin C |
 3.4.21.78 | more |
the enzyme may function as a common component necessary for lysis of target cells by cytotoxic T-lymphocytes and natural killer cells |
 3.4.21.78 | more |
TSP-1 has the capacity to stimulate B lymphocytes for proliferation in the absence of antigen |
 3.4.21.78 | more |
overview: possible roles of granzyme A: 1. involvement in T or NK cell-mediated cytolysis, 2. in extravasation of T-lymphocytes, 3. in regulation of B cell growth, 4. in control of viral infection |
 3.4.21.78 | more |
by cleaving a variety of basement membrane-associated substrates, granzyme A may disintegrate the supramolecular structure of subendothelial basement membranes in a way that allows a more rapid emigration of activated T-cells |
 3.4.21.78 | more |
extracellular enzyme is delivered to the cytosol by perforin, where it causes a rapid increase in reactive oxygen species and mitochondrial transmembrane potential loss, but does not cleave bid or cause apoptotic factor release. Mitochondrial effect is direct, does not require cytosol, and is insensitive to bcl-2 and caspase inhibition. Mitochondrial damage is an essential first step in killer cell granule-mediated pathways of apoptosis |
 3.4.21.78 | more |
compared with granzyme B, granzyme A is minor effector of target cell lysis by natural killer cells |