3.4.21.79: granzyme B
This is an abbreviated version!
For detailed information about granzyme B, go to the full flat file.
Word Map on EC 3.4.21.79
-
3.4.21.79
-
perforin
-
t-cells
-
cd8
-
cytolytic
-
immunotherapy
-
vaccine
-
lymphoma
-
rejection
-
tnf
-
dendritic
-
cell-mediated
-
ifn-gamma
-
allograft
-
tregs
-
tia-1
-
fasl
-
foxp3
-
autologous
-
interferon-gamma
-
caspases
-
degranulation
-
allogeneic
-
epstein-barr
-
antigen-specific
-
virus-specific
-
immunophenotype
-
ctla-4
-
anti-cd3
-
tumor-infiltrating
-
nk-cell
-
extranodal
-
elispot
-
synthesis
-
eomes
-
graft-versus-leukemia
-
cd45ro
-
alcls
-
biotechnology
-
death-1
-
analysis
-
intragraft
-
lag-3
-
hiv-specific
-
medicine
-
diagnostics
-
degradation
-
alloreactive
-
lymphocyte-mediated
-
lymphokine-activated
-
crma
-
b-mediated
-
pharmacology
-
ag-specific
-
banff
-
hepatosplenic
-
anti-pd-1
-
interleukin-15
- 3.4.21.79
- perforin
- t-cells
- cd8
-
cytolytic
-
immunotherapy
- vaccine
- lymphoma
-
rejection
- tnf
- dendritic
-
cell-mediated
- ifn-gamma
-
allograft
-
tregs
- tia-1
- fasl
- foxp3
-
autologous
- interferon-gamma
-
caspases
-
degranulation
-
allogeneic
-
epstein-barr
-
antigen-specific
-
virus-specific
-
immunophenotype
-
ctla-4
-
anti-cd3
-
tumor-infiltrating
-
nk-cell
-
extranodal
-
elispot
- synthesis
-
eomes
-
graft-versus-leukemia
-
cd45ro
-
alcls
- biotechnology
-
death-1
- analysis
-
intragraft
- lag-3
-
hiv-specific
- medicine
- diagnostics
- degradation
-
alloreactive
-
lymphocyte-mediated
-
lymphokine-activated
- crma
-
b-mediated
- pharmacology
-
ag-specific
-
banff
-
hepatosplenic
-
anti-pd-1
- interleukin-15
Reaction
preferential cleavage: -Asp-/- >> -Asn-/- > -Met-/-, -Ser-/- =
Synonyms
Asp-ase, C11, CCP1, CCPII, CTLA1, CTSGL1, Cytotoxic cell proteinase-1, cytotoxic lymphocyte-associated protease, cytotoxic lymphocyte-specific protein, cytotoxic serine protease granzyme B, cytotoxic T-lymphocyte-associated gene transcript-1, gB, Gra-b, granzyme B, Granzyme G, Granzyme H, GrB, GrzmB, GzB, Gzm, Gzm B, GzmB, GzmB-like enzyme, GzmH, HLp, Human lymphocyte protein, Lymphocyte protease, natural killer cell protease 1, pro-apoptotic serine protease, proGrB, Proteinase, CCP1, rat grB[N66Q], SECT, T-cell serine protease 1-3E
ECTree
Advanced search results
Application
Application on EC 3.4.21.79 - granzyme B
Please wait a moment until all data is loaded. This message will disappear when all data is loaded.
analysis
biotechnology
-
engineering of mutant enzyme suitable for cleavage of fusion proteins
degradation
diagnostics
increased detection of the enzyme in cytotoxic T lymphocytes and natural killer cells are an immune signature for lymphocyte activation in hemophagocytic lymphohistiocytosis, irrespective of genetic subtype, and may also be a useful measure of immune activation in other related conditions
medicine
pharmacology
synthesis
-
expression system for the production of high yields of enzymatic and biologically active human grB by transfection of HEK-293 with grB. The HEK-293 host cells are protected from apoptotic cell death by fusing an inactivation site coupled to a (His)6 tag to the gene sequence of GrB. Inactive grB which is actively released from HEK-293 cells by insertion of a Igkappa leader sequence is purified on a nickel column utilizing the (His)6 tag. After enterokinase digestion and heparin affinity chromatography, high yields of enzymatic and biologically active human grB are obtained
additional information
-
caution in the design and interpretation of experiments using GrBs from different species due to distinct tetrapeptide specificities and abilities to recruit the BID pathway
analysis
-
caution in the design and interpretation of experiments using GrBs from different species due to distinct tetrapeptide specificities and abilities to recruit the BID pathway
-
human and murine GzmB are distinct enzymes with different substrate preferences. Subtle differences in enzyme structure can radically affect substrate selection. Caspases are essential for apoptosis initiated by mouse GzmB
degradation
-
human and murine GzmB are distinct enzymes with different substrate preferences. Subtle differences in enzyme structure can radically affect substrate selection. Caspases are not essential for apoptosis initiated by human GzmB
-
cytolytic T-lymphocytes from enzyme or granzyme A deficient mice similarly induce early proapoptotic features such as phosphatidyl serine exposure on plasma membrane, or reactive oxygen radical generation, though with distinct kinetics. Cytolytic T-lymphocytes from granzyme A, but not granzyme B deficient animals activate caspase 3 and 9. All granzyme-induced apoptotic features depend critically on perforin
medicine
-
A streptolysin-O/GrB combination results in the induction of p53 accumulation and transcriptional activity associated with strong induction of apoptotic cell death in T1 cells
medicine
-
activated mast cells contribute, via secreted gzmB, to cell death, increased vascular permeability, leukocyte extravasation and subsequent inflammatory processes in affected tissues. GzmB-induced detachment of adherent mouse embryonic fibroblasts leads to anoikis. GzmB induces a disorganization of endothelial cell-cell contacts
medicine
-
can induce rapid apoptosis of target cells, which is dependent on caspase activation and mitochondrial damage. GzmH-induced death is characterized by phosphatidylserine externalization, nuclear condensation, DNA fragmentation, caspase activation and cytochrome c release. GzmH may play an essential role in caspase-dependent pathogen clearance in the innate immunity that may complement the proapoptotic function of GzmB in human natural killer cells
medicine
-
detection of target GzB activity followed by caspase 3 activation provides a unique readout of a potentially lethal injury delivered by cytotoxic lymphocytes
medicine
-
ELISPOT measurements of granzyme B permit the identification of actively ongoing CD8+ cell responses. Importance for immune diagnostic of infections, transplantation, allergies, autoimmune diseases, tumors and vaccine development
medicine
-
expression of granzyme B by peripheral CD8+ T lymphocytes does not vary between emphysematous smokers, smokers and non-smokers with normal lung function
medicine
-
extension of the present standard of IFN-gamma measurements to the analysis of GzB and perforin release in functional T cell assays will provide new insights into CD8+ effector T cell function in HIV infection
medicine
-
granzyme B may play a key role in ateromatous diseases. Role in cardiac allograft vasculopathy and atherosclerosis
medicine
-
granzyme B may play a key role in ateromatous diseases. Role in cardiac allograft vasculopathy and atherosclerosis
medicine
-
granzyme B plays a role in the cytotoxic response in lichen planus. It is a probable target for future immunomodulator therapy
medicine
-
granzyme H participates in the anti-adenovirus response by both inhibiting virus replication directly and simultaneously re-sensitizing infected cell to granzyme B-induced cell death
medicine
-
granzymes can mediate antiviral activity through direct cleavage of viral substrates. Different granzymes have synergistic functions to outflank viral defenses that block host antiviral activities
medicine
-
GrB proteolysis of Hsc70/Hsp70-interacting protein is important to the efficiency of death induction
medicine
-
GzmH induces cell death, it is nearly as potent as GzmB. Exhibits an alternative cell death pathway in innate immunity. In contrast to GzmB, GzmH achieves cell death by acting on mitochondrial and nuclear targets but not through the activation of hallmark apoptotic substrates
medicine
-
Hsp70/Hsp90-organizing protein per se does not set the threshold for susceptibility to GzmB-induced apoptosis
medicine
-
key role of plasticity in the granzyme B mediated cell death pathway in the killing of changed tumor cells, resulting in keratoacanthoma regression through apoptosis or direct damage of tumor cells. Insufficient activation of cytotoxic T lymphocytes and decreased release or activity of granzyme B may be responsible for squamous cell-carcinoma progression and occasional aggressive behavior in keratoacanthomas. Targeted delivery of granzyme B to squamous cell, carcinoma cells may be a new agent that may have an additive or synergic effect with conventional therapeutic modalities, since there are still no known cellular resistance mechanisms capable of protecting cells against all granzyme B mediated pathways
medicine
-
pleiotropic pro-apoptotic function of gzmB presumably to counteract evasion strategies of pathogens and to control tumors
medicine
-
Treg cells derived from the tumor environment can induce NK and CD8(+) T cell death in a granzyme B- and perforin-dependent fashion. Granzyme B and perforin are relevant for Treg cell-mediated suppression of tumor clearance in vivo
medicine
-
extracellular granzyme B may help control localized coagulation during inflammation
medicine
-
granzyme B level may contribute to a diagnosis of immune-mediated epilepsy including Rasmussen syndrome
medicine
-
granzyme B may be the limiting factor in adaptive regulatory T cell-mediated K562 target cell killing
medicine
-
plasma granzyme B level on day 14 is a significant predicting factor for left ventricular remodeling after acute myocardial infarction
medicine
-
potential role for granzyme B in the process of initiation of myasthenia gravis
medicine
-
the release of granzyme B through two routes from unconjugated cytotoxic lymphocytes suggests that it functions outside the cell and may contribute to pathology in cases of immune dysregulation, such as familial hemophagocytic lymphohistiocytosis
medicine
-
granzyme B GrB labels a subpopulation of effector cells involved in ongoing cytotoxic action should be considered as a specific marker showing the extent of the direct local cytotoxic damage in patients with lupus erythematosus
medicine
-
modified versions of GzmB with lower isoelectric points can be utilized without loss of apoptosis-inducing potential but fewer side activities
medicine
-
since GzmB is very effective in killing human tumor cell lines that are resistant against cytotoxic drugs GrzmB is used as an effector domain in potential immunoconjugates
medicine
-
both GzmA and GzmB levels are significantly increased in serum of patients with patients with amyotrophic lateral sclerosis. There is a significant correlation of serum GzmB levels with severity of clinical state of amyotrophic lateral sclerosis patients
medicine
-
granzyme B-deficient mice, and to a lesser extent perforin-deficient mice, exhibit a significant increase in the number of Ag-specific CD8+ T cells in the lungs and draining lymph nodes of virally infected animals. Viral titers in granzyme B-deficient mice are similar to wild-type mice and significantly less than perforin-deficient mice. Regulatory T cells from wild-type mice express high levels of granzyme B in response to infection, and depletion of regulatory T cells from these mice results in an increase in the number of Ag-specific CD8+ T cells, similar to that observed in granzyme B-deficient mice. Granzyme B-deficient regulatory T cells display defective suppression of CD8+ T cell proliferation in vitro
medicine
-
human neurons are selectively susceptible to granzyme B isolated from cytotoxic T cell granules. In vitro, purified human GrB induces neuronal death to the same extent as the whole activated T cell population. Following internalization through various parts of neurons, GrB accumulates in the neuronal soma. Within the cell body, GrB diffuses out of endosomes possibly through a perforin-independent mechanism and induces subsequent activation of caspases and cleavage of a-tubulin. Inhibition of caspase-3, a substrate for GrB, significantly reduces GrB-mediated neurotoxicity. Treatment of neurons with mannose-6-phosphate prevents GrB entry and inhibits GrB-mediated neuronal death
medicine
-
internalization of grB by membrane Hsp70 positive tumor cells is dependent on mammalian glycosylation of GrB. Neuraminic acid blocks binding of GrB to CT26 tumor cells
medicine
-
ischemic brain samples after stroke contain significantly higher levels of Gra-b and interferon-gamma inducible protein-10 than non-ischemic controls. In stroke, poly(ADP-ribose) polymerase-1 and heat shock protein-70 are cleaved to canonical proteolytic signature fragments by Gra-b. Gra-b also binds to Bid and caspase-3 and colocalizesw with Annexin-V+/TUNEL+ in degenerating neurons. Gra-b inhibition protects both normal and ischemia-reperfused neurons against in vitro neurotoxicity mediated by activated CG-SH cells and supernatants. Increased leukocyte infiltration and elevated Gra-b levels in the post-stroke brain can induce contact-dependent and independent post-ischemic neuronal death to aggravate stroke injury
medicine
-
proinflammatory gzmA and anti-inflammatory gzmB are novel modulators of the Th1/2 balance and defense in helminth infection
medicine
-
the precursor frequency and cytotoxic lymphocyte activity of HLA-A2-restricted transaldolase 168-176-specific CD8+ T cells is increased in multiple sclerosis patients. The major C-terminal GrB cleavage product of transaldolase, residues 28-337, has no enzymatic activity but retains the antigenicity of full-length transaldolase, effectively stimulating the proliferation and cytotoxic lymphocyte activity of peripheral blood mononuclear cells and of CD8+ T cell lines from patients with multiple sclerosis. Sera of multiple sclerosis patients exhibit similar binding affinity to wild-type and GrB-cleaved transaldolase
medicine
-
The soluble granzyme B levels are higher in systemic lupus erythematosus patients and associated with various clinical features like reduced complement components, C3 and C4, and skin lesion. The soluble granzyme B levels are also sturdily related with severity of the disease. Excessive secretion of soluble granzyme B and enhanced activity of cytotoxic T lymphocyte may play a vital role in the pathogenesis of systemic lupus erythematosus and organ damage
medicine
the protease may be a therapeutic target for the prevention of bacterial sepsis without affecting immune control of the pathogen
medicine
-
Treg cells derived from the tumor environment can induce NK and CD8(+) T cell death in a granzyme B- and perforin-dependent fashion. Granzyme B and perforin are relevant for Treg cell-mediated suppression of tumor clearance in vivo
-
medicine
-
the protease may be a therapeutic target for the prevention of bacterial sepsis without affecting immune control of the pathogen
-
granzyme B has antimalarial activity against Plasmodium falciparum strain 3D7A of 1600 nM and can be targeted delivered by a granzyme B-single-chain Fv fusion protein, inhibitory activities on parasite growth of different fusion proteins on two different Plasmodium falciparum strains, overview
pharmacology
antimalarial activity of granzyme B and its targeted delivery by a granzyme B-single-chain Fv fusion protein. Therapeutic efficacies of recombinant antibody-mediated antimalarial immunotherapeutics based on granzyme B, overview
pharmacology
functionalized superparamagnetic iron oxide nanoparticles (SPIONs) have emerged as potential clinical tools for cancer theranostics. GrB-functionalized SPIONs act as a contrast enhancement agent for magnetic resonance imaging and induce specific tumor cell apoptosis. Combinatorial regimens employing stereotactic radiotherapy and/or magnetic targeting are found to further enhance the therapeutic efficacy of GrB-SPIONs in different tumor mouse models. GrB-SPIONs accumulate in the tumor and increase MR contrast enhancement. The therapeutic potential of a systemic administration of GrB-SPIONs is evaluated in o.t. xenograft H1339 lung cancer model with and without brain metastases and U87 glioma mouse models, overview
-
cytotoxic granule-mediated death of both primary and transformed beta cells requires granzyme B. Early cell death is completely dependent on granzyme B. Death induced by granzyme B is dependent on cosecretion with perforin
additional information
Equine granzyme B shows close proximity to putative equine mast cell protease and to granzyme B from mouse, rat, and human. Equine granzyme B may be useful in the development of immunological assays for the activity of equine lymphocytes
additional information
-
Equine granzyme B shows close proximity to putative equine mast cell protease and to granzyme B from mouse, rat, and human. Equine granzyme B may be useful in the development of immunological assays for the activity of equine lymphocytes
additional information
-
role for granzyme B in the dismantling of the cytoskeleton. In the execution phase of apoptosis it may modify key structural proteins thus enabling the cell to be properly dismantled and eliminated by phagocytosis
additional information
-
ability of gzmH to cleave host proteins involved in essential viral functions provides a novel mechanism by which granzymes can mediate direct antiviral activities