Mouse Anti-Human CD256
- Known as:
- Mouse Antibody toHuman CD256
- Catalog number:
- 129-10126
- Product Quantity:
- 25
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Mouse Anti-Human CD256
Related genes to: Mouse Anti-Human CD256
- Gene:
- TNFSF13 NIH gene
- Name:
- TNF superfamily member 13
- Previous symbol:
- -
- Synonyms:
- APRIL, CD256
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2017-03-02
Related products to: Mouse Anti-Human CD256
Related articles to: Mouse Anti-Human CD256
- Immunoglobulin A (IgA) nephropathy is a common kidney disease. The cytokines B-cell Activating Factor (BAFF) and A Proliferation-Inducing Ligand (APRIL) have key roles in the pathophysiology of IgA nephropathy. Atacicept is an antibody to BAFF and APRIL. An interim analysis of atacicept in a phase 3 trial in IgA nephropathy, has shown it reduces proteinuria with a good safety profile. This is a very promising finding, and long-term results with atacicept, and a similarly promising BAFF and APRIL inhibitors, telitacicept and povetacicept in nephropathy are eagerly awaited. Of particular interest is whether long-term suppression of immunoglobulins with these inhibitors has adverse effects. Further trials will be needed to determine the respective roles of these inhibitors with angiotensin converting enzyme inhibitors (ACEi) and/or angiotensin receptor blockers (ARBs) and/or sodium-glucose cotransporter 2 (SGLT 2) inhibitors in IgA nephropathy. - Source: PubMed
Publication date: 2026/09/11
Doggrell Sheila A - Atherosclerosis (AS), a complex age-related disease characterized by arterial lipid plaque formation, remains poorly understood at the molecular level. Senescent cells, particularly macrophages, drive plaque progression, but key senescence-inducing genes and their mechanisms are unclear. - Source: PubMed
Publication date: 2026/07/22
Lin XiaoLiang MintongZeng ShenglanChen KaiyeYang YingYu FeiZhou JiahuiTang HuiTang HanqingWen PengjuTang ShulinWu Yueheng - B-cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL) drive the galactose-deficient IgA1 (Gd-IgA1) production that underlies IgA nephropathy (IgAN). Several BAFF/APRIL-pathway inhibitors have entered randomized testing, but none has been compared head-to-head. - Source: PubMed
Publication date: 2026/08/11
Mansour NadaElbarody Ramy M FKamel Ahmed M - Among the immune mechanisms underlying the pathogenesis of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), B-lineage cells play crucial roles by producing ANCA, presenting antigens to T cells, and secreting proinflammatory cytokines. The upregulated signaling pathways of the B-cell activation factor of tumor necrosis factor family (BAFF) and a proliferation-inducing ligand (APRIL), which are broadly produced by several types of myeloid cells, contribute to the activation and survival of autoreactive B cells, leading to disease onset and relapse. Furthermore, elevated levels of soluble BAFF and APRIL persist even in patients who achieve clinical remission following conventional induction therapies such as cyclophosphamide and rituximab (RTX), resulting in the cause of relapse. Active AAV is characterized by expansions of specific phenotypes in circulating B-cell lineages, including plasmablasts and plasma cells. Conversely, reductions in transitional, memory, and regulatory B cells are observed. Significant expressions of affinity receptors binding to secreting BAFF/APRIL, including decreased BAFF receptor expression on memory B cells and transitional B cells or increased transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI) expression on transitional B cells and plasmablasts/plasma cells, are also observed during acute and remission AAV. Enhanced BAFF and APRIL signaling through these receptors, especially TACI, activates the intracellular nuclear factor-κB pathway in B cells, promoting their proliferation and ANCA production. B-cell depletion therapy using RTX is effective; however, it requires repeated administration to maintain remission, which can occasionally lead to infection. Belimumab, a BAFF-inhibiting monoclonal antibody, alone has shown limited efficacy in preventing relapse of AAV. Targeting BAFF/APRIL signaling pathways and their binding receptors, along with the downstream molecular pathways in targeted B cells, is essential for developing novel therapeutic strategies aimed at achieving complete and sustained AAV remission. - Source: PubMed
Publication date: 2026/07/21
Shimojima YasuhiroYoshida ShuheiMatsumoto HarukiSumichika YuyaAsano TomoyukiSato Shuzo - A proliferation-inducing ligand (APRIL), a ligand of B-cell maturation antigen (BCMA), might have an impact on the efficacy of BCMA CAR T-cell in multiple myeloma. Here, we found plasma concentrations of APRIL increased (> 1 nM) during the first month in patients showing responses to BCMA CAR T-cell therapies, and APRIL levels negatively correlated with soluble BCMA (sBCMA) levels. APRIL bound with sBCMA and decreased the detectability of sBCMA in ELISA detection, an effect different from γ-secretase inhibitor. APRIL also bound cell membrane BCMA but with a much lower affinity comparing with sBCMA. sBCMA bound with BCMA CAR T-cell, and decreased the binding and killing of myeloma cells by BCMA CAR T-cells in vitro. APRIL, at concentrations of 2 and 10 nM, inhibited the binding of sBCMA and BCMA CAR T-cell, and increased the binding and killing of myeloma cells by BCMA CAR T-cells. In murine xenotransplant myeloma models, giving APRIL during the first week after infusion of BCMA CAR T-cells increased IFNγ-positive CAR T-cells in the tumor tissues, and enhanced the anti-tumor effect of CAR T-cell. In conclusion, APRIL counteracted the actions of sBCMA in BCMA CAR T-cell-mediated binding and killing of myeloma cells which might contribute to the efficacy of BCMA CAR T-cell therapies. - Source: PubMed
Publication date: 2026/07/01
She HuanhuanLin JiahanZhou DianZhang XiaotianZheng FeiFeng QiaoXiao LiwenChen WeiYan ZhilingPan Bin