TNFSF13B monoclonal antibody (M19), clone 3G6
- Known as:
- TNFSF13B mab (anti-) (M19), clonality 3G6
- Catalog number:
- H00010673-M19
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- TNFSF13B monoclonal antibody (M19) clone 3G6
Related genes to: TNFSF13B monoclonal antibody (M19), clone 3G6
- Gene:
- AGMO NIH gene
- Name:
- alkylglycerol monooxygenase
- Previous symbol:
- TMEM195
- Synonyms:
- FLJ16237
- Chromosome:
- 7p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2007-11-20
- Date modifiied:
- 2016-10-05
- Gene:
- CCSER1 NIH gene
- Name:
- coiled-coil serine rich protein 1
- Previous symbol:
- FAM190A
- Synonyms:
- KIAA1680
- Chromosome:
- 4q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2009-07-09
- Date modifiied:
- 2015-11-05
- Gene:
- CCSER2 NIH gene
- Name:
- coiled-coil serine rich protein 2
- Previous symbol:
- KIAA1128, FAM190B
- Synonyms:
- -
- Chromosome:
- 10q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-27
- Date modifiied:
- 2015-11-05
- Gene:
- ERICH6 NIH gene
- Name:
- glutamate rich 6
- Previous symbol:
- C3orf44, FAM194A
- Synonyms:
- MGC39662, ERICH6A
- Chromosome:
- 3q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-01-13
- Date modifiied:
- 2015-11-05
- Gene:
- ERICH6B NIH gene
- Name:
- glutamate rich 6B
- Previous symbol:
- FAM194B
- Synonyms:
- FLJ32682
- Chromosome:
- 13q14.13
- Locus Type:
- gene with protein product
- Date approved:
- 2009-09-08
- Date modifiied:
- 2015-11-05
Related products to: TNFSF13B monoclonal antibody (M19), clone 3G6
Related articles to: TNFSF13B monoclonal antibody (M19), clone 3G6
- 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 - Myasthenia gravis (MG) presents a clinical challenge where autoantibody titers poorly predict disease severity, and thymectomy provides inconsistent benefits. We hypothesized that thymic B cells acquire survival mechanisms that bypass canonical tolerance checkpoints, enabling persistence independent of antigen-specific selection. Using single-cell RNA sequencing, V(D)J repertoire analysis, and spatial transcriptomics to generate the largest MG atlas to date (237,661 cells), we identified a tolerance checkpoint swap in MG pathogenesis. Pathological class-switched B cells within thymic germinal centers exhibited reduced antigen presentation ( and ) and diminished costimulation while up-regulating to engage BAFF-driven survival. This shift allows polyclonal autoreactive B cells to evade stringent selection and seed peripheral sites. T follicular helper cells supported this reprogramming via increased and expression, with the latter facilitating dopamine-mediated synaptic acceleration. These findings offer insight into clinical paradoxes in MG and point to the BAFF-BCMA axis as a potential therapeutic target and biomarkers for disease activity. - Source: PubMed
Publication date: 2026/08/12
Yan YuanqingPatino Diego AvellaZhao YimengWu XinBudinger G R ScottBharat Ankit - Primary cutaneous T-lymphomas (CTCL), particularly in their early stages, frequently present with clinical and histopathologic features that overlap with atopic dermatitis (AD) and psoriasis, contributing to diagnostic delay and ineffective, or even deleterious, treatment approaches. Thus, minimally invasive molecular tests capable of distinguishing CTCL from benign inflammatory dermatoses are urgently needed. - Source: PubMed
Publication date: 2026/08/07
Fleischli AbigailBar JonathanManson MeredithNg Brandon DMeledathu ShannonBurnett AmeliaChefitz GabriellaEstrada Yeriel DGour DigpalCices AhuvaCorrea da Rosa JoelBrunner Patrick MGuttman-Yassky Emma - Diffuse Gastric Cancer (DGC) is an aggressive subtype with a poor prognosis and a lack of specific biomarkers, representing a critical unmet need in oncology. This study aimed to elucidate the key molecular drivers of DGC by integrating RNA-seq data with a multi-faceted bioinformatics approach. - Source: PubMed
Publication date: 2026/08/06
Azni Zahra KhaliliBorhani Matia SadatSabouri HosseinSajadi Sayed JavadArjmand Maryam Pasandideh - 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