DTL; BAFF; BLYS; CD257; TALL1; THANK; ZTNF4; TALL-1; TNFSF20; TNFSF13B, rHuman BAFF Active
- Known as:
- DTL; BAFF; BLYS; CD257; TALL1; THANK; ZTNF4; TALL-1; TNFSF20; TNFSF13B, rHuman BAFF Active
- Catalog number:
- RF0030-100
- Product Quantity:
- 100ug
- Category:
- -
- Supplier:
- Agren
- Gene target:
- DTL; BAFF; BLYS; CD257; TALL1; THANK; ZTNF4; TALL-1; TNFSF20; TNFSF13B rHuman BAFF Active
Related genes to: DTL; BAFF; BLYS; CD257; TALL1; THANK; ZTNF4; TALL-1; TNFSF20; TNFSF13B, rHuman BAFF Active
- Gene:
- DTL NIH gene
- Name:
- denticleless E3 ubiquitin protein ligase homolog
- Previous symbol:
- -
- Synonyms:
- RAMP, L2DTL, DCAF2, CDT2
- Chromosome:
- 1q32.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-16
- Date modifiied:
- 2016-10-05
- Gene:
- TNFRSF13C NIH gene
- Name:
- TNF receptor superfamily member 13C
- Previous symbol:
- -
- Synonyms:
- BAFFR, CD268
- Chromosome:
- 22q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-05-22
- Date modifiied:
- 2019-04-23
- Gene:
- TNFSF13B NIH gene
- Name:
- TNF superfamily member 13b
- Previous symbol:
- TNFSF20
- Synonyms:
- BAFF, THANK, BLYS, TALL-1, TALL1, CD257
- Chromosome:
- 13q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-19
- Date modifiied:
- 2018-11-22
Related products to: DTL; BAFF; BLYS; CD257; TALL1; THANK; ZTNF4; TALL-1; TNFSF20; TNFSF13B, rHuman BAFF Active
Related articles to: DTL; BAFF; BLYS; CD257; TALL1; THANK; ZTNF4; TALL-1; TNFSF20; TNFSF13B, rHuman BAFF Active
- Systemic lupus erythematosus is a chronic, multisystemic, inflammatory disease. Aquaporins, a group of transmembrane channels, are known to help prime immune cells and their migration. In this study, a qRT-PCR analysis was performed to identify aquaporins whose expression in SLE patients was associated with the inflammatory profile of B cells. - Source: PubMed
Publication date: 2025/05/06
Baharlooi HusseinEnayati SamanehAhmadzadeh NooshinMadreseh ElhamFaezi Seyedeh TaherehAlikhani MajidJamshidi AhmadrezaMahmoudi MahdiFarhadi Elham - B-cell activating factor belonging to the TNF family (BAFF), also known as B-lymphocyte stimulator (BLyS), plays a crucial role in B-cell development. It has multiple receptors, including BCMA, TACI, and BAFF-R, with diverse roles in different cell types. BAFF induces B-cell proliferation and immunoglobulin secretion, and acts as a survival factor for immature, naive, and activated B cells. Consequently, BAFF-deficient mice often show suppressed humoral responses, while BAFF-overexpressing mice show the higher number of mature B cells and may develop autoimmune-like manifestations and B-cell lymphoproliferative diseases. Elevated BAFF levels are also associated with various hematological malignancies, and its expression correlates with disease progression in some cases. Therefore, BAFF-targeted therapies, such as belimumab, atacicept, and tabalumab, are being explored in clinical trials for conditions like chronic lymphocytic leukemia (CLL) and multiple myeloma. Belimumab, an anti-BAFF monoclonal antibody, is being investigated in combination with rituximab/venetoclax for CLL. Atacicept, a decoy receptor for BAFF and APRIL, showed tolerability in a phase 1b trial for CLL. Tabalumab, another monoclonal antibody targeting BAFF, did not demonstrate significant efficacy in a phase 2 study for relapsed/refractory multiple myeloma. BAFF ligand-based CAR-T cells are designed to target BAFF receptors and show promise in preclinical studies, particularly for B-cell malignancies. The review emphasizes the importance of understanding the roles of BAFF and its receptors in the microenvironment of hematologic malignancies. Targeting BAFF and its receptors presents potential therapeutic avenues, and ongoing clinical trials provide valuable insights. - Source: PubMed
Publication date: 2024/09/02
Tagami NamiYuda JunichiroGoto Yasuyuki - BAFF, a vital B cell survival and differentiation factor, has three receptors: B-cell maturation antigen (BCMA), transmembrane activator and CAML interactor (TACI) and BR3. Although B cells are greatly reduced in B6.Baff (which harbour no BAFF) and B6.Br3 mice (which harbour supra-normal levels of BAFF), the distributions of B cell subsets and relationships between Foxp3 and CD4 cells in these mice differ. Using a large panel of B6 congenic knockout and/or transgenic mice, we demonstrate that (1) supra-normal levels of BAFF per se do not explain the phenotypic differences between B6.Baff and B6.Br3 mice; (2) B cells are expanded in B6.Taci mice, with preferential expansion of follicular (FO) B cells at the expense of CD19CD21CD23 B cells but without the preferential expansion of Foxp3 cells observed in B6 mice bearing a Baff transgene; (3) despite no expansion in total B cells, percentages of FO B cells and marginal zone B cells are higher and percentages of CD19CD21CD23 B cells are lower in young B6.Bcma mice, consistent with the inability of B6.Br3.Taci mice to recapitulate the B cell profile of B6.Baff mice; and (4) percentages of Foxp3 cells in B6.Br3.Taci mice are intermediate between those in B6.Br3 and B6.Taci mice despite the B cell profile of B6.Br3.Taci mice strongly resembling that of B6.Br3 mice. Collectively, our findings point to a non-redundant role for each of the BAFF receptors in determining the ultimate lymphocyte profile of the host. This may have clinically relevant ramifications in that the degree that a candidate therapeutic agent blocks engagement of any given individual BAFF receptor may affect its clinical utility. - Source: PubMed
Publication date: 2024/08/31
Stohl WilliamWu YingStohl Malka - Chronic kidney disease (CKD) is an emerging cause for morbidity and mortality worldwide. Acute kidney injury (AKI) can transition to CKD and finally to end-stage renal disease (ESRD). Targeted treatment is still unavailable. NF-B signaling is associated with CKD and activated by B cell activating factor (BAFF) via BAFF-R binding. In turn, renal tubular epithelial cells (TECs) are critical for the progression of fibrosis and producing BAFF. Therefore, the direct involvement of the BAFF/BAFF-R system to the pathogenesis of CKD is conceivable. We performed non-accelerated nephrotoxic serum nephritis (NTN) as the CKD model in BAFF KO (B6.129S2-/J), BAFF-R KO (B6(Cg)-/J) and wildtype (C57BL/6J) mice to analyze the BAFF/BAFF-R system in anti-glomerular basement membrane (GBM) disease using high throughput RNA sequencing. We found that BAFF signaling is directly involved in the upregulation of collagen III as BAFF ko mice showed a reduced expression. However, these effects were not mediated via BAFF-R. We identified several upregulated genes that could explain the effects of BAFF in chronic kidney injury such as , , , , , and . Thus, we conclude that targeted treatment with anti-BAFF drugs such as belimumab may reduce chronic kidney damage. Furthermore, upregulated genes may be useful prognostic CKD biomarkers. - Source: PubMed
Publication date: 2024/05/16
Möckel TamaraBoegel SebastianSchwarting Andreas - Hidradenitis suppurativa (HS) is a chronic inflammatory disease characterized by painful inflamed nodules, abscesses, and pus-draining tunnels appearing in axillary, inguinal, and perianal skin areas. HS lesions contain various types of immigrated immune cells. - Source: PubMed
Publication date: 2022/12/05
Sabat RobertŠimaitė DeimantėGudjonsson Johann EliBrembach Theresa-CharlotteWitte KatrinKrause TorbenKokolakis GeorgiosBartnik EckartNikolaou ChristosRill NataschaCoulibaly BémaLevin ClémentHerrmann MatthiasSalinas GabrielaLeeuw ThomasVolk Hans-DieterGhoreschi KamranWolk Kerstin