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anti-Mouse (Murine) GZMA Antibodies:
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Human Monoclonal GZMA Primary Antibody for FACS, IP - ABIN2689529
Barry, Heibein, Pinkoski, Lee, Moyer, Green, Bleackley: Granzyme B short-circuits the need for caspase 8 activity during granule-mediated cytotoxic T-lymphocyte killing by directly cleaving Bid. in Molecular and cellular biology 2000
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Human Monoclonal GZMA Primary Antibody for IHC (p), WB - ABIN2473883
Mayne, Allen, Bowell: 'Partial D' women with anti-D alloimmunization in pregnancy. in Clinical and laboratory haematology 1992
Show all 4 Pubmed References
Human Polyclonal GZMA Primary Antibody for WB - ABIN4316050
Bem, Bos, Bots, Wolbink, van Ham, Medema, Lutter, van Woensel: Activation of the granzyme pathway in children with severe respiratory syncytial virus infection. in Pediatric research 2008
Human Polyclonal GZMA Primary Antibody for ELISA - ABIN4274922
Martinvalet, Dykxhoorn, Ferrini, Lieberman: Granzyme A cleaves a mitochondrial complex I protein to initiate caspase-independent cell death. in Cell 2008
GzmA and gzmB were predominantly expressed by natural killer cells, and during abdominal sepsis, the percentage of these cells expressing gzms in peritoneal lavage fluid decreased, while the amount of expression in the gzm(+) cells increased
a novel endogenous trigger for autoimmune diabetes and an in vivo role for granzyme A in maintaining immune tolerance.
this study shows that gzmA and gzmB partly regulate local inflammation during early pneumonia but eventually play an insignificant role during pneumosepsis by the common human pathogen Klebsiella pneumoniae
Granzyme A does not have a crucial role in vivo in the protective response to tuberculosis.
Data indicate N-terminomics on the human and mouse granzymes A and K by combined fractional diagonal chromatography (COFRADIC).
The results, in susceptible B6 mice for GzmB and in resistant 129/Sv mice for GzmA and/or the GzmB cluster, point to granzyme-mediated host defense regulation in the liver in experimental visceral leishmaniasis.
Estrogen increases the extracellular expression and interleukin (IL)-12-induced activity of a critical member of serine protease family granzyme A.
functional divergence between human and mouse granzyme A
We have demonstrated that cell death can be induced when mGzmA is delivered by primary natural killer cells via authentic Cytotoxic lymphocyte/target cell interactions.
Regulated secretion of granzyme A and cytotoxic killing was enhanced and correlated with increased vesicle-associated membrane protein 7 availability.
GzmA deficiency in filarial infection is linked with reduced inflammation and a trend toward increased alternatively activated macrophages.
granzyme A- and B-cluster deficiency delays the acute progression of pneumovirus disease by reducing alveolar injury.
the genes for perforin, the three major T cell granzymes (A-C) and IFN-gamma are differentially expressed during primary activation of naive CD8(+) T cells, kinetically and at the single-cell level
granzyme A and granzyme B have a similar potential to induce rapid perf-mediated apoptosis but that their individual contribution to the underlying intracellular process is dictated by the quality of the target cell
NK cell mediated tumor control is dependent on granzymes.
some cytolytic T lymphocytes mature into perforin/granzyme-expressing effector cells in the mediastinal lymph node and are detectable when they accumulate in lung infection
In all tumor models examined thus far, granzyme A is not necessary for tumor rejection mediated by the perforin pathway in vivo.
gzmA and gzmB induce multiple independent cell death pathways; all gzm-induced apoptotic features analyzed depend critically on perf.
polymorphonuclear leukocytes from mice and humans lack the 3 cytotoxic effector molecules, gzmA, granzyme B, and perforin, generally associated with natural killer and cytotoxic T lymphocytes
IL-2 increased the expression of perforin and granzyme A, B, and C mRNA; induction of granzyme A, B, and C mRNA required exogenous IL-2, whereas induction of perforin and IFN-gamma expression did not.
GzmA produced by lesional CD8 T cells has the capacity to specifically increase chemokine secretion from inflamed keratinocytes, thereby sustaining the focal inflammation in psoriasis lesions by amplifying a chemotactic inflammatory loop.
granzyme A in human platelets increases with aging
GzmA plays an unfavorable role in host defense during pneumococcal pneumonia by a mechanism that does not depend on natural killer cells.
Carbamate pesticides significantly reduced the intracellular levels of perforin, GrA, GrB, Gr3/K, and GRN in NK-92CI cells.
Our results suggest that granzyme A could be considered another biomarker of TB, that can be used, other than IFN-gamma, to discriminate between patients with active TB and LTBI subjects
Delivered into parasite infected cells by granulysin and perforin, granzymes generate superoxide and inactivate oxidative defense enzymes to kill the parasite.
Taken together, the authors verified that histone H3 is a real substrate for GzmA in vivo in the Raji cells treated by staurosporin.
Results reveal enhanced intra- and extracellular expression of gzmA and B in patients with pulmonary TB, suggesting that gzms are part of the host response to tuberculosis.
Levels of GZMA and ITGAE mRNAs in colon tissues can identify patients with UC who are most likely to benefit from etrolizumab; expression levels decrease with etrolizumab administration in biomarker(high) patients.
GzmA and GzmB expressing cells in the airways and lung parenchyma was higher in subjects who died from asthma
GZMA, GBP5 and CD64 genes show promise as a rapid diagnostic markers separating tuberculosis from other pulmonary diseases.
We herewith identify GZMA as critical effector molecule of human Treg function for gastrointestinal immune response in an experimental GvHD model.
The exocytosed granzyme A enters target cells and mediates IL-1beta maturation independently of caspase-1 and without inducing cytotoxicity.
Serum concentrations of granzyme A in patients with ovarian cancer were substantially increased in comparison to concentrations in patients with ovarian cystadenomas or ovarian teratomas.
Patients with chronic immune thrombocytopenia have elevated serum granzyme A levels.
A critical and previously unsuspected role is revealed for granzymes A and B in dictating immunogenicity by influencing the mode of tumor cell death.
The results indicate that GzmA and GzmB are implicated in mechanisms of neurodegeneration in amyotrophic lateral sclerosis.
investigation of substrate specificity toward Jurkat cell proteins; more than 260 cleavage sites, almost exclusively favoring basic residues at the P1 position, in approximately 200 unique protein substrates, were identified
Cytolytic T lymphocytes (CTL) and natural killer (NK) cells share the remarkable ability to recognize, bind, and lyse specific target cells. They are thought to protect their host by lysing cells bearing on their surface 'nonself' antigens, usually peptides or proteins resulting from infection by intracellular pathogens. The protein described here is a T cell- and natural killer cell-specific serine protease that may function as a common component necessary for lysis of target cells by cytotoxic T lymphocytes and natural killer cells.
, Granzyme A
, BLT esterase
, H factor
, Hanukah factor
, autocrine thymic lymphoma granzyme-like serine protease
, serine esterase 1
, t cell-specific serine protease 1
, CTL tryptase
, Granzyme A (Cytotoxic T-lymphocyte-associated serine esterase-3; Hanukah factor serine protease)
, cytotoxic T-lymphocyte proteinase 1
, h factor