BAFFR Blocking Peptide
- Known as:
- BAFFR Blocking Peptide
- Catalog number:
- 33r-10814
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- BAFFR Blocking Peptide
Related genes to: BAFFR Blocking Peptide
- 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
Related products to: BAFFR Blocking Peptide
Related articles to: BAFFR Blocking Peptide
- TB meningitis (TBM) has up to 50% mortality in people living with HIV. We investigated differences in cerebrospinal fluid (CSF) host immune responses associated with short-term mortality. - Source: PubMed
Publication date: 2026/06/18
Louine MartineauDandekar RaviReddy Sumanth PKaralius Mary CWaldrop GreerWang ShiyinGakuru JaneKimuda SarahMugabi TimothyMusubire Abdu KKagimu EnockAbassi MahsaKabahubya MableWilliams Darlisha APhan Hoang VanDai BiyueZia MahamZorn Kelsey CFouassier CamilleGerungan ChloeMarra Pedro SSkipper Caleb PBahr Nathan CLangelier Charles RCreswell Fiona VBoulware David RMeya David BWilson Michael R - The neurotoxicity mechanisms of tetrachloro-1,4-benzoquinone(TCBQ) remain poorly understood. This study integrated computational simulations validation to elucidate TCBQ-induced neurotoxicity. - Source: PubMed
Publication date: 2026/06/09
Rong ChunshuWei ZhenXie DongeWang QingyuanRen HaoxuWang XuZhao Dexi - : Pancreatic adenocarcinoma (PAAD) is a highly aggressive malignancy with limited treatment options and a poor prognosis. Extracellular vesicles (EVs), which play a central role in intercellular communication, have emerged as promising non-invasive biomarkers for both diagnosis and prognosis. This study aimed to identify EV-related genes, construct a more accurate prognostic model using data from multiple databases, and explore the functional roles of key genes in PAAD. : Four publicly available datasets, PAAD_ExoRbase, TcgaTargetGtex-PAAD, GSE62452_GPL6244, and GSE78229_GPL6244, were analyzed, leading to the identification of 40 differentially expressed EV-related genes. Using the Least Absolute Shrinkage and Selection Operator (LASSO) Cox regression, five prognostic genes, , , , , and , were selected to construct a nomogram model for predicting patient outcomes. Single-cell analysis showed that these five genes were expressed in T-proliferative, malignant, and ductal cells. Analyses of immune cell infiltration and immune checkpoints further supported the model's prognostic performance. The regulatory role of the key gene was validated in an in-house cohort and confirmed through in vitro experiments and RNA sequencing. Furthermore, analyses of conditioned medium, EV isolation and characterization, and endothelial tube formation assays demonstrated that EVs derived from CFPAC-1 cells carrying enhanced PAAD angiogenesis through VEGF/VEGFR signaling. - Source: PubMed
Publication date: 2026/05/01
Ma TianyinGongye XiangdongDongzhi CairangMa ShuxianChai YiboGuo Wing-WaWang QikunTian Ming - Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of methotrexate-associated lymphoma arising in immune deficiency/dysregulation (MTX-associated IDD-DLBCL) among rheumatoid arthritis patients treated with MTX and is characterized by frequent spontaneous regression (SR) after MTX withdrawal. However, some patients do not achieve SR and have poor outcomes. Epstein-Barr virus (EBV) infection correlates with frequent SR but does not fully explain clinical heterogeneity. We investigated prognostic factors irrespective of EBV infection status. We analyzed 21 MTX-associated IDD-DLBCL cases applying the nCounter PanCancer Immune Profiling Panel and immunohistochemistry (IHC) to identify predictors of non-SR cases. Ten patients were classified as SR and 11 as non-SR. Gene expression profiling revealed higher expression of CD83, ICOSLG, IL21R, BCL6, CD40, PAX5, CXCR5, CD79A, DMBT1, and TNFRSF13C in non-SR cases. We therefore focused on CD83, which showed the highest fold change and the most significant P value among these markers. Although CD83 is reported to be a surface marker of mature dendritic cells, IHC analysis revealed that CD83 was more frequently expressed on tumor cells than on dendritic cells. High CD83 IHC positivity (≥15%) in tumor cells correlated with mRNA levels and predicted non-SR after MTX withdrawal. Multivariate analysis identified CD83 IHC high expression as an independent predictor of non-SR cases. High CD83 expression is an independent prognostic factor in MTX-associated IDD-DLBCL, and combined evaluation may refine risk stratification and guide clinical decisions. - Source: PubMed
Sawada KeisukeTakahashi TakumiFukumura YukiOnagi HirokoAshizawa KarinYamashita TakahisaYamamoto WataruTakayanagi NatsukoAdachi AkikoKashimura MakotoTabayashi TakayukiTamaru Jun-IchiHigashi MorihiroMomose Shuji - Systemic lupus erythematosus (SLE) is a chronic and refractory autoimmune disease characterized by multi-organ damage, for which reliably safe and effective treatment remains an unmet need. Autoantibodies, secreted by autoreactive B cells, deposition is the central pathogenesis of organ damage in SLE. Current studies reported B cell receptor and B cell activating factor (BAFF)-mediated signals regulate the activation and survival of B cells and production of autoantibodies. We showed that marginal zone B cells and CD11cT-bet autoreactive B cells expressed higher levels of BAFF receptor and BTK in MRL/lpr mice. Here, a liposome-delivery system capable of targeting BAFFR autoreactive B cells by conjugating anti-BAFFR antibody on the surface of the PEG-liposomes and loading BTK-inhibitor ibrutinib (BTEL) was rationally designed. Notably, the BTEL nanoparticles could inhibit the survival and activation of B cells, and systemic administration of BTEL could alleviate the development of the lupus mouse model by decreasing the production of anti-dsDNA autoantibodies, along with reduced secretion of inflammatory cytokines and kidney damage, and without apparent side effects. These findings suggest the potential of BTEL in targeting autoreactive B cells, blocking signaling pathways, and improving the efficacy of BTK inhibitors, providing a promising therapeutic approach for SLE, while also reducing toxicity. - Source: PubMed
Publication date: 2026/01/11
Zhang YaminWen JingjingJiang BilingJiang HaoXu JianTao Juan