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Validated All-in-One™ qPCR Primer for GZMB(NM_004131.5) Search again
Product ID:
HQP008690
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
C11, CCPI, CGL-1, CGL1, CSP-B, CSPB, CTLA1, CTSGL1, HLP, SECT
Gene Description:
granzyme B
Target Gene Accession:
NM_004131.5(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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 encoded by this gene is crucial for the rapid induction of target cell apoptosis by CTL in cell-mediated immune response. [provided by RefSeq].
Gene References into function
- expressed during acute cellular rejection episodes after kidney transplantation
- A comparison of proforms and mature forms of granzyme B in regulating granulopoiesis
- most WT1- and proteinase 3-reactive CD8 T-cells observed in patients with acute myeloid leukemia were granzyme B(+).
- expression of granzyme B in plasmacytoid dendritic cells
- proapoptotic granzyme is exocytosed predominantly as a macromolecular complex with serglycin
- Sequence analysis of this gene do not support it as a candidate gene for familial hemophagocytic lymphohistiocytosis.
- Results suggest that cell-mediated cytotoxicity during HIV-1 infection may be impaired due to a deficient quantity of active granule proteins such as granzyme B or to their abnormal regulation.
- granzyme B initiates caspase processing but cannot fully process procaspase-3 in intact Jurkat T leukemia or NT2 neuronal cells
- granzyme B mediates direct cleavage of caspase 3 and also activates mitochondrial disruption, resulting in the release of proapoptotic proteins that suppress caspase inhibition
- GrB expression is present in normal human articular chondrocytes and elevated in rheumatoid arthritis chondrocytes
- Expressed in blood as a marker of kidney transplantation rejection.
- Granzyme B is a caspase-like serine protease that is released by cytotoxic lymphocytes to kill virus-infected and tumor cells.
- PMNs contain perforin and granzyme B, the 2 molecules known as the cytotoxic entity of natural killer cells and of cytotoxic T lymphocytes
- granzyme B leakage-induced cell death is an important determinant of activation-induced NK cell death.
- These results suggest that the main pathway of cytotoxic T lymphocyte-mediated apoptosis in peptic ulcer formation is the perforin/granzyme pathway irrespective of H. pylori infection.
- Levels predict acute rejection in small intestine transplants.
- serglycin-bound granzyme B in high-molecular-weight degranulate material from cytotoxic T lymphocytes predominantly followed a dynamin-dependent pathway to kill target cells
- the RAH allele represents a neutral polymorphism in the GrB gene; it retains pro-apoptotic activity
- expression levels of granzyme B mRNA was significantly higher in the patients undergoing acute rejection as compared to patients with stable lung function
- examined the correlation between injury of the hepatocytes and mRNA expression of FasL and perforin/granzyme B in liver tissue to investigate the roles of both the FasL and the perforin/granzyme B pathways in chronic hepatitis B
- Mcl-1L degradation by either GrB or caspase-3 interferes with Bim sequestration by Mcl-1L
- granzyme H complements the pro-apoptotic function of granzyme B in human NK cells
- results demonstrate discordant expression of granzymes A and B in human lymphocyte subsets and T regulatory cells, which suggests that different granzymes may play unique roles in immune system responses and regulation
- proteinase inhibitor 9 was effectively hydrolyzed and inactivated by human granzyme M, raising the possibility that this orphan granzyme bypasses proteinase inhibitor 9 inhibition of granzyme B
- cell surface heparan sulfate-bound GzmB was taken up rapidly into intracellular lysosomal compartments; blocking treatments had no an inhibitory influence on induced apoptosis
- granzyme B targets a highly restricted range of substrates and orchestrates cellular demolition largely through activation of caspase-3
- Patients with disease flares were characterized by higher proportions of perforin- and/or granzyme B-positive lymphocytes with a differentiated effector phenotype (CCR7- and CD45RA+).
- expression of proteinase inhibitor-9 and granzyme B mRNAs may be controlled through different pathways
- Data show that granzyme B directly cleaves ROCK II, and that this causes constitutive kinase activity and bleb formation.
- mechanism of delivery is proposed entailing electrostatic transfer of granzyme B from serglycin to cell surface proteins
- etiologic agent of Kawasaki Disease interferes with expression of this cytotoxic protein by CD8 T lymphocytes, prolonging inflammation in the arterial wall and leading to coronary artery aneurysm formation.
- determination of role in cell detachment in immortalized and transformed cell lines as well as normal cell lines
- Cytotoxic T-lymphocyte precursor frequency can be determined by the granzyme B and interferon gamma marker for determining donor-specific cytolytic activity after clinical organ transplantation.
- polymorphonuclear leukocytes from mice and humans lack the 3 cytotoxic effector molecules, granzyme A, gzmB, and perforin, generally associated with natural killer and cytotoxic T lymphocytes
- In an electrostatic "exchange-adsorption" model, cationic sites participate in binding of GrB to the cell surface, thereby promoting its uptake and eventual release into the cytoplasm
- Mice lacking funcitonal MST1R are suceptible to acute lung injury and have increased expression of granzymes in the lung, thymus and spleen
- Intracellular and extracellular effects of human GrB in tumor cell lines using recombinant protein expressed in the yeast Pichia pastoris.
- granzyme B directly attacks a major component of the cell cytoskeleton, which may contribute to the incapacitation of target cells during CTL/NK-mediated killing
- UV-B induces GrB and PFN expression in keratinocytes, and these cells acquire acquire a significant cytotoxicity, which is GrB and PFN dependent, toward a variety of cellular targets.
- granzyme B is released from cytolytic granules to the cytosol of CD8(+) T lymphocytes upon CD3/Receptors, Antigen, T-Cell stimulation and escapes protease inhibitor 9, thereby mediating apoptotic cell death
- identified a novel NF-kappaB binding site, which plays a pivotal role in controlling human granzyme B gene transcription
- GrB/scFvMEL, a fusion protein composed of human granzyme B (GrB) and the single-chain antibody scFvMEL, targets melanoma gp240 antigen and exerts impressive cytotoxic effects by inducing apoptosis.
- granzyme B is a novel mediator of allergic diseases
- PCR analysis for Granzyme B/perforin up-regulation might play a role along with clinical criteria for detection of presymptomatic acute rejection episodes in intestinal recipients.
- data revealed significantly increased number of t-cells expressing granzyme B in rKA compared to SCC, suggesting a possible role of granzynme B in KA regression
- discovery of a new inhibitor of granzyme B and a new mechanism used by Sertoli cells for immunoprotection
- Results suggest that perforin and granzyme-B gene expressions are accurate in detecting both cellular and antibody-mediated rejection.
- loss of PI9 expression in tumor cells may reflect some mechanism associated with progression
- Mouse granzyme B is 30 times less cytotoxic than human granzyme B and does not require Bid for killing but regains cytotoxicity on engineering of its active site cleft. Mouse granzyme A is considerably more cytotoxic than human granzyme A.
- cleavage and release to the extracellular milieu of the GluR3B peptide may in principle increase its antigenicity
- granzyme B is induced by ultraviolet A rays in human keratinocytes through MIF
- TNFalpha- and FasL-stimulated acute myeloid leukemia cell lytic induction is regulated by a signalling pathway involving sequentially, radical oxygen species generation, Trx oxidation, ASK1 activation, p38MAPK stimulation and GrB induction.
- These data demonstrate that human and murine GzmB are distinct enzymes with different substrate preferences. Our observations also illustrate how subtle differences in enzyme structure can radically affect substrate selection.
- perforin and granzyme B expressing cells in lichen sclerosis were found in the dermal infiltrate and intraepidermally in close proximity to keratinocytes suggesting in situ activation of these cells
- Granzyme B is expressed and released by human mast cells upon physiologic stimulation.
- Cytotoxic molecule (CM) expression, specifically TIA1 and granzyme B, is predictive of prognosis in Hodgkin's-like anaplastic large cell lymphoma.
- Patients with high levels of circulating granzyme B had lipid-rich carotid plaques as determined by echogenicity and had more ischemic lesions on cerebral MRI
- Hip is a pro-survival substrate of granzyme B
- Detection of target granzyme B activity followed by caspase 3 activation provides a unique readout of a potentially lethal injury delivered by cytotoxic lymphocytes.
- Ex vivo ELISPOT measurements of granzyme B permit the identification of actively ongoing CD8(+) cell responses-a notion that is pertinent to the immune diagnostic of infections, transplantation, allergies, autoimmune diseases, tumors, vaccine development
- Show increased granzyme B positive cytotoxic T-lymphocytes in inflamed mucosa of patients with inflammatory bowel disease.
- The results indicated that the high expression of NKG2A/CD94 and low expression of granzyme B may be related with the reduced activity of cord blood NK cells.
- Granzyme B, on one hand might, enhance the cytotoxic potential of PMN, on the other, it may provide PMN with additional means to degrade extracellular matrices.
- The ratio of FOXP3+ regulatory T-cells to granzyme B+ cytotoxic T/NK Cells predicts prognosis in classical Hodgkin lymphoma.
- We report on a frequent ex vivo dissociation of the HIV peptide-induced secretion of perforin, granzymeB and IFN gamma by HIV-specific CD8(+) cells in HIV infection.
- The genes PRF1, GZMB, UNC13D, and Rab27a involved in hemophagocytic lymphohistiocytosis do not confer a significant risk of association with systemic-onset juvenile idiopathic arthritis.
- Report activation of the granzymeA/B pathway in children with severe respiratory syncytial virus infection.
- Accessible chromatin-associated (histone 3 lysine 9) acetylation state serves as a cornerstone for differentially high expression of effector gene eomesodermin and its targets perforin 1 and granzyme B in memory CD8 T cells.
- In cervical carcinomas, high pre-treatment GZMB level was associated with poor response to therapy.
- Granzyme B and perforin are diagnostic molecular markers of acute rejection. Granzyme B and perforin blood levels are also increased in viral infections and posttransplant lymphoproliferative disease.
- The potential role for GrB in the process of initiation of myasthenia gravis, and are consistent with the concept of an immunodominant epsilon epitope of acetylcholine receptors.
- In a cell-based system GzmB-deficient natural killer cells provided perforin (pfn) by natural polarized secretion and synergized with externally added GzmB
- Granzyme B induces apoptosis of chondrocytes with natural killer cell-like cytotoxicity in rheumatoid arthritis
- five genes (TNFSF10/TRAIL, IL1RN, IFI27, GZMB, and CCR5) were upregulated and three genes (CLK1, TNFAIP3 and BTG1) were downregulated in at least three out of four subpopulations during acute GVHD.