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
Ask about this productRelated 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
- Bovine leukemia virus (BLV) is an oncogenic deltaretrovirus that establishes lifelong infection in cattle and may progress from asymptomatic carriage to persistent lymphocytosis (PL) and lymphoma. Although adaptive immune alterations have been widely studied, the stage-specific transcriptional landscape of innate immunity in BLV infection remains incompletely defined. In this study, we performed a targeted innate immune transcriptomic analysis using RNA-seq data derived from 18 Holstein dairy cows selected from a screened population of 130 animals in Querétaro, Mexico. Animals were classified into three groups based on serology, proviral load, and hematological criteria: BLV-seronegative controls (n = 5), asymptomatic BLV-infected cattle (AL), and BLV-infected cattle with PL. Total peripheral blood leukocytes were subjected to RNA extraction and sequencing on the Illumina NovaSeq platform. Differential gene expression analysis was conducted using DESeq2 with significance defined as adjusted P-value (padj) < 0.05 and |log fold change|≥ 1. A curated panel of innate immune-related genes encompassing pattern recognition receptors, interferon signaling, inflammatory mediators, inflammasome components, and cytotoxic effectors was analyzed. Comparison between Control and Asymptomatic cattle identified 8 genes that were significantly altered (padj < 0.05). Asymptomatic animals demonstrated upregulation of antiviral and immune-regulatory genes, including EIF2AK2 (logFC = 1.10, padj = 0.011), KLRK1 (logFC = 0.98, padj = 0.009), and IL18 (logFC = 0.77, padj = 0.015), indicating activation of interferon-associated and inflammatory pathways. Marked upregulation of TNFRSF13C (logFC = 3.25, padj = 0.046) and TNFAIP3 (logFC = 2.03, padj = 0.049) suggests modulation of B-cell survival signaling and NF-κB regulatory control. In contrast, NCR1 (logFC = - 1.04, padj = 0.044), LMX1B (logFC = - 0.80, padj = 0.030), and TNFSF12 (logFC = - 0.78, padj = 0.044) were downregulated, reflecting selective adjustment of cytotoxic and TNF superfamily pathways. PL animals exhibited broader innate immune transcriptional alterations consistent with sustained inflammatory activation. These findings demonstrate that asymptomatic BLV infection is characterized by controlled activation of antiviral and regulatory innate immune pathways, whereas disease progression toward PL is associated with expanded inflammatory reprogramming. Stage-specific innate immune signatures may therefore contribute to viral persistence and clinical outcome in BLV-infected cattle. - Source: PubMed
Publication date: 2026/10/07
Akbarin Mohammad MehdiFarjami ZahraAcevedo-Jiménez Gabriel EduardoMurillo Cecilia RodríguezGonzález-Fernández Víctor Davidde María Ávila-De la Vega LuceroÁlvarez Hugo Ramírez - Mitochondrial outer membrane permeabilization (MOMP) is a core apoptotic regulatory event that dictates mitochondrial integrity, where full activation drives cell death and sublethal dysregulation contributes to tumor genomic instability. We used the Cancer Genome Atlas lung adenocarcinoma cohort (TCGA-LUAD) as the training cohort and the Gene Expression Omnibus dataset GSE42127 as the validation cohort to identify prognostic genes related to MOMP activity in lung adenocarcinoma (LUAD) and to evaluate their potential biological significance. By intersecting MOMP-related genes with differentially expressed genes, combined with survival analysis, Mendelian randomization analysis, and 101 machine-learning algorithm combinations, seven prognostic genes, namely BIRC5, PSMD11, TNFRSF13C, YWHAZ, YWHAG, CYCS, and LTB, were identified. Next, an optimal prognostic model was constructed based on the gradient boosting machine (GBM) algorithm. Based on the risk score, LUAD patients were stratified into high- and low-risk groups, and patients in the high-risk group exhibited poorer overall survival in both the training and validation cohorts. Furthermore, a nomogram integrating the risk score and clinicopathological factors was developed and showed favorable predictive performance for 1-, 3-, and 5-year survival. Meanwhile, functional and immune analyses revealed that the high-risk group was enriched in DNA replication-related pathways and demonstrated a higher tumor mutation burden (TMB). Correlation analysis indicated that TNFRSF13C was positively correlated with activated B cells, whereas BIRC5 was negatively correlated with eosinophils, suggesting that MOMP-related genes might be involved in remodeling the immune microenvironment of LUAD. Drug sensitivity analysis showed differences in predicted half-maximal inhibitory concentration (IC50) values between the risk groups, suggesting the potential value of this model in assisting therapeutic stratification. Single-cell RNA sequencing (scRNA-seq) further identified T lymphocytes as a key cell type, with numerous prognostic genes exhibiting differential expression in T cells or dynamic changes during differentiation. We suggest that the MOMP-related signature established in this study may provide a reference for prognostic stratification in LUAD and offers candidate prognostic genes for subsequent experimental and clinical validation. - Source: PubMed
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Liu DongmeiHe BinchanZhou XuanYang YuemeiSong MengyueXu Xiaoyong - Single-chain antibody-based CAR-T cells targeting BAFF-R have demonstrated antitumor effects against human B-cell malignancies and can overcome CD19 antigen loss. However, CARs built on antigen-specific single-chain antibody variable fragments may have limitations, e.g., large CAR binding domain size. To improve the function of BAFF-R CAR-T cells, we designed CARs with only a fully human heavy-chain variable domain. - Source: PubMed
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