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Validated All-in-One™ qPCR Primer for TNFSF13B(NM_006573.4) Search again
Product ID:
HQP090914
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BAFF, BLYS, CD257, DTL, TALL-1, TALL1, THANK, TNFSF20, TNLG7A, ZTNF4
Gene Description:
TNF superfamily member 13b
Target Gene Accession:
NM_006573.4(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
The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This cytokine is a ligand for receptors TNFRSF13B/TACI, TNFRSF17/BCMA, and TNFRSF13C/BAFFR. This cytokine is expressed in B cell lineage cells, and acts as a potent B cell activator. It has been also shown to play an important role in the proliferation and differentiation of B cells. [provided by RefSeq].
Gene References into function
- interacts with newly identified receptor BAFF-R, which appears to be the principal receptor for BAFF-mediated mature B cell survival
- BAFF may play a role in the development of T cell responses, in addition to its role in B cell homeostasis.
- Levels of BLyS protein were, on average, threefold higher in patients with follicular lymphoma compared to normal donors
- crystal structure of the TNF-homologous domain
- determined the three-dimensional crystal structure of BLyS to 2.0 A resolution and identified receptor recognition segments using limited proteolysis coupled with mass spectrometry
- BAFF is a survival and maturation factor for mouse B cells
- 10 genes, including interleukin (IL)-10, lymphocyte activation gene-1 (LAG-1), GCP-2, PBEF, ferritin, PIM-2, TFG, CD27 ligand, DUSP5, and archain, were up-regulated at the mRNA level by TALL-1 stimulation in B lymphoma cells and/or primary B lymphocytes.
- BLyS and APRIL critically link the innate and adaptive immune responses.
- aberrantly expressed by B chronic lymphocytic leukemia cells
- When coexpressed with APRIL, BLYS forms active heterotrimeric molecules that circulate in the serum of patients with systemic immune-based rheumatic diseases.
- REVIEW: role in regulating the peripheral B cell compartment and humoral immunity, and the contribution of altered BLyS expression to B lymphocyte diseases
- Review. BLyS is one of the most important cytokines of the TNF superfamily. It supports normal B-cell function & promotes B-cell autoimmunity.
- macrophage- and DC-derived BAFF is a key molecule by which macrophages and DCs directly regulate human B-cell proliferative responses to T-cell-independent stimuli.
- crystal structure and interactions with BAFF receptor
- BAFF/BLyS receptor 3 comprises a minimal TNF receptor-like module that encodes a highly focused ligand-binding site.
- BAFF may enhance humoral immunity in vivo by promoting survival of Ig-secreting cells via a B cell maturation antigen-dependent mechanism
- alternative splicing of the BAFF gene regulates receptor binding and biopresentation of the B cell survival cytokine, BAFF
- B-CLL cells can be rescued from apoptosis through an autocrine process involving BAFF, APRIL, and their receptors.
- BAFF up-regulates activation-induced cytidine deaminase and enhances class-switch DNA recombination in Epstein-Barr virus-infected B cells.
- BAFF may play an important role in FDC-B-cell interactions through the B-cell coreceptor complex and a possibly sequential link between the T cell-independent and -dependent B-cell responses in the germinal centers.
- Dysregulation of BLyS over extended periods of time is common in patients with systemic lupus erythematosus
- Exposure of non-Hodgkin's lymphoma B cells to recombinant or myeloid cell-derived BAFF attenuates apoptosis, increases NF-kappa B activation, up-regulates Bcl-2 and Bcl-xL, and down-regulates Bax.
- serum levels of BAFF and APRIL were increased about 5-fold in patients with multiple myeloma as compared with healthy donors
- Antagonissts may provide treatment for systsemic lupus erythematosus (REVIEW)
- BLyS and its receptors represent a potentially important therapeutic target in B-cell lymphoma
- novel mechanism that might dramatically exacerbate the release of BLyS by neutrophils during pathologic inflammatory responses.
- Review. BLyS plasma levels in systemic lupus erythematosus, Sjogren's syndrome & rheumatoid arthritis are higher in patients than controls. BLyS may have a role in the interaction between the monocyte & the B lymphocyte in some autoimmune disease.
- another form of TACI exists wherein the N-terminal cysteine-rich domain (CRD) is removed by alternative splicing and is capable of ligand-induced cell signaling and that the second CRD alone (TACI_d2) contains full affinity for both APRIL and BAFF
- The induced expression of BAFF on fibroblast-like synoviocytes by proinflammatory cytokines in vitro may enhance the capacity of such cells to protect B cells from apoptosis in inflammatory microenvironments in vivo.
- Macrophages promote Burkitt's lymphoma cell survival through a B-cell survival factor (BAFF)-dependent mechanism.
- show that the main site of production for BAFF and APRIL is the bone marrow (BM) environment, and that production is mainly by monocytes and neutrophils. In addition, osteoclasts produce very high levels of APRIL, unlike BM stromal cells
- BAFF transgene overexpression in vivo promotes delayed-type hypersensitivity, which is a classical type 1 T-helper (Th1) cell response, and suppresses Th2-dependent allergic airway responses.
- conclude that BAFF and APRIL from NLCs can function in a paracrine manner to support leukemia cell survival via mechanisms that are distinct from those of SDF-1alpha
- Serum levels of sBAFF and sAPRIL were increased in Sjogren's syndrome, especially in anti-Ro/La+ patients
- The known effect of B cells in periodontitis would be partly mediated by salivary BAFF in patients with primary Sjogren's syndrome.
- BLyS regulates B cell as well as T cell function and has pro- and antiinflammatory activities in rheumatoid arthritis.
- In Wagener's granulomatosis (WG) patients, serum levels of BAFF are significantly increased, therefore BAFF is proposed to be a possible pathogenic factor in WG.
- B cell homeostasis is maintained by BAFF-mediated regulation of Bcl-2-binding protein, BIM.
- BLyS was found to increase the viability and proliferation of malignant B cells from Waldenstrom macroglobulinemia patients.
- Full-length BLyS and DeltaBLyS mRNA levels are elevated in systemic lupus erythematosis and are more closely associated with disease activity than are BLyS protein levels.
- Ala134-BAFF is more efficacious than myc-Gln136-BAFF in inducing B cell proliferation. Formation of the 60-mer in solution by BAFF extracellular domain is an intrinsic property of the protein. This more active form of BAFF may be physiologically relevant
- NFKB and NFAT regulate BLyS expression via at least one NFKB and 2 NFAT BLYS promoter binding sites. Constitutive activation of NFKB and BLyS in NHL-B cells forms a positive feedback loop associated with lymphoma cell survival and proliferation
- BAFF gene polymorphism is neither involved in genetic predisposition to primary Sjogren's syndrome nor associated with a specific pattern of antibody production.
- Chronic activation of B cells through this CD40-independent pathway could impair protective T cell-dependent antibody responses by inducing immune exhaustion
- results indicated that four residues, H218, F220, T228 and L229, are indispensable for the biological activity of cBLyS, whereas two regions, amino acid 134-148 and amino acid 271-285, are related to the biological activity of BLyS.
- The addition of Qn to previous therapeutic regimens in active SLE is beneficial and seems to reduce SLEDAI scores, serum BAFF and aCL levels and therefore should be considered in many of our SLE patients before aggressive treatments are given.
- expression of BAFF was regulated through a signal transduction pathway which involves c-jun NH2-terminal kinase and p38
- BAFF (the assistance of which is required for proper transformation of transitional TI B cells into transitional TII B cells) accumulated adjacent to transitional and marginal-zone-like B lymphocytes in Sjogren's syndrome.
- BAFF secretion is 3- to 10-fold higher in bone marrow stromal cell than in multiple myeloma cells; tumor cell adhesion to BMSCs augments BAFF secretion by 2- to 5-fold, confirmed by both ELISA and immunoblotting.
- high BLyS production is often correlated with certain inflammatory autoimmune diseases and B-lymphocyte malignancies
- patients with CVID were screened using DHPLC and direct sequencing: No disease causing mutations were identified. A novel heterozygous single nucleotide polymorphism(G189A), which does not lead to an amino acid substitution, was found in one individual.
- BR3, which is expressed on all mature B cells, is a specific receptor for the B-cell survival and maturation factor BAFF.
- BAFF has provided considerable new insight into B cell homeostasis and immune function, and represents an important new molecular target for treatment of autoimmune diseases and lymphomas--{REVIEW}
- Review. The splice variants, binding specificities, structural determinants for ligand selectivity, and signaling pathways are reviewed.
- Review. BAFF is required for mature B cell development and survival but causes B cell hyperplasia and autoimmunity when it is overexpressed.
- Review. Defects in the production of BAFF and/or expression of its receptors have been associated with a diverse array of human immunopathologies characterised by perturbed B cell function and behaviour, like autoimmunity, malignancy, & immunodeficiency.
- Review. BLyS signaling via BR3 is the dominant homeostatic regulator of primary B cell pools.
- Review. Signal cascades that effect BLyS- dependent survival, regulation of BLyS signaling, BLyS as a growth factor & BLyS- induced metabolic enhancement in B cell response to BCR and TLR-dependent signaling.
- Review. BAFF and its receptor have roles in B cell biology outside of a survival mechanism. These include germinal center maintenance, isotype switching, and regulation of specific B cell surface markers.
- Review. Direct BAFF/APRIL signalling in T cells and/or T cell modulation in response to a BAFF-modified B cell compartment may play an important role in inflammation and immunomodulation.
- recombinant gelonin/B lymphocyte stimulator fusion toxin may have potential therapeutic efficacy for B-CLL patients
- These results indicated that the recombinant BAFF mutants modified with Th epitopes could induce neutralizing antibodies against BAFF in vivo.
- B-lymphocyte stimulator (BLyS) plays a critical role in the survival of B-lymphocytes and has a role in progression of Hodgkin's lymphoma
- BAFF levels are elevated in the serum of autoimmune patients--{REVIEW}
- anti-BAFF IgG might amend deleterious effects of BAFF in B-cell-mediated autoimmune diseases
- These data define a complex role for BAFF in humoral immune responses and show for the first time that BAFF can also play an inhibitory role in B cell differentiation.
- The timing of B cell repopulation in rituximab-treated Sjogren's syndrome patients is modulated by BAFF and is followed by reconstitution of the preexisting abnormalities.
- As neutrophils enter the site of inflammation, they release surface-expressed BLyS in a TNFalpha-dependent manner, and thus may contribute to local stimulation of autoimmune B cell responses.
- Peripheral blood mononuclear cells of CVID subjects had increased levels of BAFF mRNA.
- results suggest that BAFF contributes to liver injury and disease development in autoimmune hepatitis patients
- BAFF playsan important role in the pathogenesis of idiopathic thrombocytopenic purpura by activating B cells.
- suggest a model for the pathology of endometriosis where BLyS-responsive plasma cells interact with retrograde menstrual tissues to give rise to endometriosis lesions
- Low levels of the BAFF TVs in all lymphocyte subpopulations analyzed suggest that their main source in PBMC are monocytes.
- Results suggest that elevated serum APRIL and BAFF levels are differentially associated with disease severity in systemic sclerosis.
- findings indicate that BAFF secretion by resident cells in target organs of autoimmunity is tightly regulated by innate immunity, with positive and negative controls, depending on the receptors and the pathways triggered
- BAFF has a role as a survival factor in multiple myeloma
- TACI supported survival of activated B cells and plasmablasts in vitro
- BAFF has a role in B-cell activation in patients with active chronic graft-versus-host disease
- IFNalpha activity and BAFF levels are elevated in the plasma of patients with Sjogren's syndrome compared with healthy controls.
- All of these results indicated that the abnormally high expression of BAFF on T lymphocytes from MPE may play a role of anti-tumor effect.
- These findings indicate a previously unreported role for the BAFF/BAFF-R pair in mature B-cell chemotaxis.
- Elevated BAFF and APRIL expression levels might partially reflect the common immunological feature of primary antibody deficiency.
- BAFF inhibits Fas-mediated cell death, however, the BCR-driven survival signals were not strengthened by BAFF, therefore, BAFF may function independently of the antigen specificity of BCR.
- The roles of BAFF protein and interferon gamma in IgA production of tonsillar mononuclear leukocytes in patients with IgA nephropathy.
- serum BAFF is elevated and appears to play an important role in the development of alopecia areata
- BAFF induction by target organs of autoimmune diseases after viral infection may be a link between innate immunity and autoimmunity
- the constant expression of BAFF, in adipocytes, normal breast cells and their cancer counterparts, might be relevant of the trophic potency in breast, promoting the proliferation and development of normal and malignant breast tissue.
- there are potential autocrine and paracrine pathways for BAFF and APRIL signaling in human placentas suggest that lineage-specific regulation of placental cell viability, differentiation and/or other activities may be novel functions of these proteins
- Overproduction of BAFF in nasal polyps may contribute to the pathogenesis of chronic rhinosinusitis with nasal polyps
- data suggest that BLyS may modulate adaptive immune cells indirectly by inducing dendritic cell maturation
- Elevated BAFF (B-cell activating factor) in a subset of ERA patients is related to autoantibody levels and synovitis
- In certain patients, inflammatory microenvironment provides BAFF-dependent paracrine survival signal to B-cells in TLOs, allowing them to escape rituximab-induced apoptosis, thereby thwarting therapeutic efficiency.
- only feature characterizing familial CLL patients was a higher serum BAFF level (sporadic CLL 336 ng/mL, range 93-925; familial CLL 601 ng/mL, range 138-8914; P=0.002). Our data suggest that BAFF levels are elevated in patients with familial CLL
- viral dsRNA may initiate frontline IgG and IgA responses through an innate TLR3-dependent pathway involving BAFF
- BAFF might play a role in the immunopathogenesis of myasthenia gravis.
- These results provide a mechanism by which Fcgamma receptors can elevate circulating BLyS levels and promote autoantibody production in immune complex-mediated autoimmune diseases.
- susceptibility for Ro/La-positive primary Sjogren's syndrome (pSS) is increased with the CTAT haplotype, but not with high s-BAFF levels; elevated s-BAFF in pSS are associated with the TTTT haplotype & may be a secondary phenomenon in Ro/La-positive pSS
- Report bioassay for human BAFF based on expression of a mouse BAFF-receptor ectodomain-human tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor-2 endodomain fusion receptor in human rhabdomyosarcoma cells.
- Autocrine BAFF signal transduction pathways may contribute to Helicobacter pylori-independent growth of gastric DLBCL (MALT).
- overexpression of IFN-gamma in peripheral blood T cells contributes to the immunopathogenesis of systemic lupus erythematosus via the induction of sBLyS by monocytes/macrophages
- Circulating BLyS levels and systemic lupus erythematosus (SLE) are positively correlated. BLyS is a candidate for therapeutic targeting in SLE.
- hsBAFF results in the elevation of NK cell activity by regulation of CD4(+) T lymphocytes contributing to IL-2 and IFN-gamma generation
- BAFF is a good biomarker for IFN-beta response, and requires further studies to determine its value as a marker for clinical response and NAb predisposition.
- There are elevated levels of BAFF and APRIL in cerebrospinal fluid of systemic lupus erythematosus (SLE) patients. APRIL was augmented in neuropsychiatric SLE patients compared with SLE patients without central nervous system involvement.
- We propose that an aberrant BAFF/BAFF-R-dependent autocrine mechanism may play a role in the development of certain types of nonhematopoietic cancer cells.
- Human BLyS facilitates engraftment of human PBL derived B cells in immunodeficient mice
- non-Hodgkin's B lymphoma cell adhesion to bone marrow stromal cells augmented BAFF secretion twofold through upregulation of BAFF gene expression, protecting lymphoma cells from apoptosis.
- We report that BAFF levels are increased in patients with autoimmune MG. Our data suggest that BAFF is likely to play a role in the pathogenesis of MG by promoting the survival and maturation of autoreactive B cells.
- investigation of the role of BAFF promoter polymorphism in HCV-related mixed cryoglobulinemia patients as a genetic contributor to its pathogenesis
- BAFF might contribute to autoimmunity and disease development in ITP. However, BAFF serum level must be carefully considered as a surrogate marker of disease activity in ITP.
- Serum BAFF (B-cell activating factor )levels were elevated in patients with active Behcets disease compared to the healthy controls, and correlated positively with the extent of skin lesions.
- BLyS serum levels significantly increase, independent of SNPs rs12428930, rs12583006, rs1224141, & rs9514828), after rituximab therapy. These high levels may promote the proliferation of residual malignant B-cells explaining rituximab failure.
- These results indicate that BAFF may be involved in the development of graft-loss and influences the long-time outcome of kidney allograft, likely mediated by interfering with immune response.
- T cell responses in BAFF-transgenic mice are profoundly compromised, as indicated by their acceptance of islet allografts and delayed skin graft rejection.
- The antigen-induced production of BAFF in the airway might contribute to local class-switch recombination and immunoglobulin synthesis by B cells.
- Case Report: Elevation of B cell-activating factor belonging to the tumour necrosis family family (BAFF) in haemophilia A patients with inhibitor.