3.4.21.78: granzyme A
This is an abbreviated version!
For detailed information about granzyme A, go to the full flat file.
Word Map on EC 3.4.21.78
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3.4.21.78
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thrombospondin-1
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angiogenesis
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endothelial
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perforin
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killer
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granule
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angiogenic
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antiangiogenic
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cytolytic
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matricellular
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metastasis
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collagen
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microvessels
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t-cells
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microvascular
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integrins
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fibrosis
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fibronectin
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cd8
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tgf-beta1
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neovascularization
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fasl
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fgf-2
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corneal
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alphavbeta3
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exocytosis
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ctl-mediated
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factor-beta
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bfgf
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medicine
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caspase-independent
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angiogenesis-related
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granule-associated
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integrin-associated
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angiostatic
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proangiogenic
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metronomic
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properdin
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endostatin
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granulysin
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tregs
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lymphocyte-mediated
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lymphokine-activated
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ifn-gamma
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vegf-a
- 3.4.21.78
- thrombospondin-1
- angiogenesis
- endothelial
- perforin
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killer
- granule
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angiogenic
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antiangiogenic
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cytolytic
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matricellular
- metastasis
- collagen
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microvessels
- t-cells
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microvascular
- integrins
- fibrosis
- fibronectin
- cd8
- tgf-beta1
- neovascularization
- fasl
- fgf-2
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corneal
- alphavbeta3
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exocytosis
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ctl-mediated
- factor-beta
- bfgf
- medicine
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caspase-independent
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angiogenesis-related
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granule-associated
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integrin-associated
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angiostatic
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proangiogenic
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metronomic
- properdin
- endostatin
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granulysin
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tregs
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lymphocyte-mediated
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lymphokine-activated
- ifn-gamma
- vegf-a
Reaction
Hydrolysis of proteins, including fibronectin, type IV collagen and nucleolin. Preferential cleavage: -Arg-/-, -Lys-/- >> -Phe-/- in small molecule substrates =
Synonyms
Autocrine thymic lymphoma granzyme-like serine protease, CTL tryptase, CTLA3, Cytotoxic T lymphocyte serine protease, GrA, Gzm A, Gzma, GzmA/K, H factor, Hanukkah factor, HuTPS, T-cell associated protease 1, T-cell derived serine proteinase 1, TSP-1
ECTree
3.4.21.78 granzyme AAdvanced search results
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results (Substrates Products
Substrates Products on EC 3.4.21.78 - granzyme A
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SUBSTRATE 
PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
Reversibility
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
Abz-GLFRSLSS(K-dnp)D + H2O
Abz-GLFR + SLSS(K-dnp)D
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a quenched fluorescence peptide substrate
-
-
?
Abz-VANRSAS(Kdnp)D + H2O
Abz-VANR + SAS(Kdnp)D
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a quenched fluorescence peptide substrate
-
-
?
benzyloxycarbonyl-Gly-Arg thiobenzyl ester + H2O
benzyloxycarbonyl-Gly-Arg + phenylmethanethiol
Boc-Trp-Arg-SBzl + H2O
?
-
thioester substrate, recombinant granzyme A
-
?
D-(epsilon-Benzyloxycarbonyl)Lys-Pro-Arg 4-methylcoumarin 7-amide + H2O
?
-
-
-
-
?
H-D-Pro-Phe-Arg p-nitroanilide + H2O
H-D-Pro-Phe-Arg + p-nitroaniline
i.e. S2302, measurement of enzymatic activity of granzyme A activity in lysates of CD8+ TAL
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-
?
Ku70 double strand break repair protein + H2O
?
-
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cleavage of Ku70 after R301, disrupting Ku complex binding to DNA and blocking of Ku70 antiapoptotic functions, cleavage of Ku70 after R301, disrupting Ku complex binding to DNA
-
?
N-acetyl-Ile-Glu-Pro-Asp p-nitroanilide + H2O
N-acetyl-Ile-Glu-Pro-Asp + p-nitroaniline
measurement of enzymatic activity of granzyme A activity in lysates of CD8+ TAL
-
-
?
Nalpha-benzyloxycarbonyl-Lys-SBzl + H2O
Nalpha-benzyloxycarbonyl-Lys + phenylmethanethiol
-
-
-
?
Precursor of interleukin-1beta + H2O
Interleucin-1beta
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i.e. pIL-1beta, cleavage at Arg120
-
?
3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide + H2O
?
MTT, benzyloxy-carbonyl-Lys-thiobenzyl ester, standard MTT-assay measuring loss of mitochondrial respiration, interspecies differences of granzyme A between human and mouse analyzed, different cytotoxic potential identified
-
-
?
3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide + H2O
?
MTT, benzyloxy-carbonyl-Lys-thiobenzyl ester, standard MTT-assay measuring loss of mitochondrial respiration, interspecies differences of granzyme A between human and mouse analyzed, mouse granzyme A is considerably more cytotoxic than human granzyme A
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-
?
benzyloxycarbonyl-Gly-Arg thiobenzyl ester + H2O
benzyloxycarbonyl-Gly-Arg + phenylmethanethiol
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-
-
-
?
benzyloxycarbonyl-Gly-Arg thiobenzyl ester + H2O
benzyloxycarbonyl-Gly-Arg + phenylmethanethiol
-
-
-
-
?
benzyloxycarbonyl-Lys-thiobenzyl ester + H2O
benzyloxycarbonyl-Lys + phenylmethanethiol
-
-
-
-
?
benzyloxycarbonyl-Lys-thiobenzyl ester + H2O
benzyloxycarbonyl-Lys + phenylmethanethiol
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-
-
-
?
Boc-Ala-Ala-Arg-SBzl + H2O
?
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thioester substrate, recombinant granzyme A
-
?
D-Pro-Phe-Arg 4-nitroanilide + H2O
D-Pro-Phe-Arg + 4-nitroaniline
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low or no activity against peptide synthetic substrates carrying other amino acid sequences at position P2, P3 adjacent to L-arginine or against substrates in which amino acids other than L-arginine are bound to the nitroanilide group
-
?
histone H4 + H2O
?
histone H4 is a substrate for GzmA in staurosporine-induced cells
-
-
?
histone H4 + H2O
?
the histone H4 N-terminal tail is cleaved by GzmA, the enzyme cleaves only deacetylated histone H4
-
-
?
N-alpha-benzyloxycarbonyl-Arg-SBzl + H2O
?
-
thioester substrate, recombinant granzyme A
-
?
PHAPII + H2O
?
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HLA-associated protein, cleaved by the recombinant enzyme at nanomolar concentrations
-
?
protein NDUFS3 + H2O
?
-
GzmA cleavage of native Ndufs3 disrupts complex I electron transport
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-
?
protein NDUFS3 + H2O
?
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GzmA accesses the mitochondrial matrix to cleave the complex I protein NDUFS3, an iron-sulfur subunit of the NADH:ubiquinone oxidoreductase complex I, after Lys56 to interfere with NADH oxidation and generate superoxide anions. NDUFS3 is cleaved in cells treated with GzmA and perforin in a dose-dependent manner. Human GzmA cleaves both human and mouse NDUFS3. GzmA induces caspase-independent increased reactive oxygen species
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-
?
additional information
?
-
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the enzyme may function as a common component necessary for lysis of target cells by cytotoxic T-lymphocytes and natural killer cells
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-
?
additional information
?
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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
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-
?
additional information
?
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most abundant protease in cytotoxic T lymphocytes, granzyme A pathway of cell-mediated cytotoxicity, produced as proenzyme, activated by the dipetidyl exopeptidase cathepsin C
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?
additional information
?
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most abundant protease in cytotoxic T lymphocytes, granzyme A pathway of cell-mediated cytotoxicity, produced as proenzyme, activated by the dipetidyl exopeptidase cathepsin C
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?
additional information
?
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compared with granzyme B, granzyme A is minor effector of target cell lysis by natural killer cells
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-
?
additional information
?
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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
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-
?
additional information
?
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extracellular substrates of granzyme A and proposed functions summarized, pathological consequences of extracellular granzyme A in disease reviewed, role of anionic interactions in extracellular substrate binding summarized, evidence for the role of glycosaminoglycan-binding sites of granzyme A in extracellular matrix remodelling described
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-
?
additional information
?
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interspecies differences of granzyme A between human and mouse analyzed by 51Cr-release assay, different cytotoxic potential identified
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-
?
additional information
?
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interspecies differences of granzyme A between human and mouse analyzed by 51Cr-release assay, different cytotoxic potential identified
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-
?
additional information
?
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studies on sensitivity to granzyme A-mediated cell death in chilblain lupus patients, less sensitivity to granzyme A-mediated apoptosis in cells carrrying the heterozygous missense mutation D18N in the 3'-5' DNA repair exonuclease TREX1
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-
?
additional information
?
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study to analyze importance of granzyme A in development of chronic obstructive pulmonary disease (COPD)
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-
?
additional information
?
-
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study to analyze importance of granzyme A in development of chronic obstructive pulmonary disease (COPD)
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-
?
additional information
?
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study to analyze the role of granzyme A in development of chronic obstructive pulmonary disease (COPD)
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-
?
additional information
?
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study to analyze the role of granzyme A in development of chronic obstructive pulmonary disease (COPD)
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-
?
additional information
?
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characterization of substrate specificity using an N-terminal peptide-centric proteomics technology. Among 260 cleavage sites, a basic residue at P1 position is favored, and P1 arginine is preferred over lysine. P4 shows a preference for Pro, Ala and Val. In P1' position, long linear amino acids with significant hydrophobic character are enriched. Gly is highly favored at P2' position. The substrate repertoires of granzyme A and granzyme B are partially overlapping
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-
?
additional information
?
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substrate specifiicty, comparison to the murine enzyme at the peptide and proteome-wide levels, overview
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-
?
additional information
?
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substrate specifiicty, comparison to the murine enzyme at the peptide and proteome-wide levels, overview
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-
?
additional information
?
-
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TSP-1 has the capacity to stimulate B lymphocytes for proliferation in the absence of antigen
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-
?
additional information
?
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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
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-
?
additional information
?
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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
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-
?
additional information
?
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substrate specificity, comparison to the human enzyme at the peptide and proteome-wide levels, overview
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-
?
additional information
?
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involvement of granzyme A in exacerbation and perpetuation of enteritis indicated, early increase of granzyme A in rats with experimentally induced ulcerative colitis shown
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-
?
