CD30L ELISA kit
- Known as:
- CD30L Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CD30L-CH
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CD30L ELISA kit
Related genes to: CD30L ELISA kit
- Gene:
- TNFSF8 NIH gene
- Name:
- TNF superfamily member 8
- Previous symbol:
- CD30LG
- Synonyms:
- CD153
- Chromosome:
- 9q32-q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-08
- Date modifiied:
- 2018-02-13
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- Multiple myeloma (MM) is a malignant plasma cell disease inducing osteolytic lesions by disrupting bone homeostasis, fostering catabolic and suppressing anabolic functions. While the impact on osteoblast generation and function is well documented, alterations of osteocyte function and extracellular matrix (ECM) are not yet fully understood. Thus, using a syngeneic mouse model of MM by injecting MOPC315.BM cells intratibially into BALB/c mice (n = 95), we performed transcriptomic profiling of an osteocyte-enriched population and identified a mechanosensitive matrisomal gene signature, which was disrupted by tumor engraftment. Non-invasive tibial loading restored the expression of 94 ECM-associated genes, including collagens, fibronectin, and aggrecan. Cross-species integration with RNA-seq data from 387 MM patients revealed eight ECM-related genes whose expression correlated with overall survival (VEGFA, BCAN, FGF13, TNFSF8, SDC1, LAMC1, SEMA3A, and CCL2). Four of these genes (Vegfa, Sdc1, Sema3a, Ccl2) were also load-responsive in a murine osteocyte (IDG-SW3 cells) bioreactor model. Our findings indicate that an existing mechanosensitive osteocytic repair program is suppressed by MM cells, which can be reinvigorated via a brief single loading session. It suggests that exercise-based interventions may be beneficial to restore bone mass through endochondral ossification programs in patients with MM. - Source: PubMed
Publication date: 2026/09/07
Ziouti FaniAzeem MuhammadRummler MaximilianRosolowski MaciejZapata GerardoRindt WyonnaJulien CatherineTauer Josephine TCheng Wen-HuiBeck SusanneSeckinger AnjaHose DirkLeich EllenBogen BjarneLynch Maureen EKuric MartinKrug MelanieEbert ReginaZaucke FrankJakob FranzWillie Bettina MJundt Franziska - Infection susceptibility and systemic infection severity arise from distinct tissue barriers and host-response compartments, but plasma-protein genetic studies often treat infection as a broad phenotype. We aimed to define a site-resolved host plasma-protein architecture of infection susceptibility across urinary, lower-respiratory, systemic, and skin/soft-tissue infection outcomes. We performed proteome-wide two-sample cis-protein quantitative trait locus (cis-pQTL) Mendelian randomization (MR) using UK Biobank Pharma Proteomics Project (UKB-PPP) instruments and registry-derived FinnGen R13 infection endpoints. Prioritized protein-outcome pairs underwent regional colocalization, prior-sensitivity analysis, Steiger-like directionality sensitivity, Finnish and broader European reference-panel linkage disequilibrium (LD) assessment, candidate-level deCODE pQTL-source follow-up where feasible, and druggability and safety-domain annotation. Across 18,766 harmonized tests, evidence was strongly site-resolved. PSCA emerged as the principal novel cystitis-specific candidate (OR 0.977, 95% CI 0.967-0.987), with strong colocalization and high Finnish reference-panel linkage disequilibrium between the MR instrument and the top colocalization single-nucleotide polymorphism (SNP) (r = 0.980). UMOD anchored urinary host-defense coherence. APOE showed strong evidence for the registry-derived implicit sepsis endpoint but was interpreted as a pleiotropy-prone broad host-response or severity-associated locus. TNFSF8 retained a robust pneumonia MR signal, but colocalization was moderate (PP.H4 = 0.544) and became weak under stringent priors (PP.H4 = 0.107), despite high-LD deCODE proxy-instrument follow-up. Skin/soft-tissue infection lacked a convergent lead. This study supports a site-resolved architecture of genetically anchored plasma-protein candidates for infection susceptibility. PSCA and UMOD define complementary urinary signals, whereas APOE and TNFSF8 require cautious interpretation as broad host-response and lower-respiratory follow-up hypotheses rather than established therapeutic targets. - Source: PubMed
Publication date: 2026/07/29
Ji ShanLi Tongzeng - Pharmacological targets supported by genetic evidence demonstrate significantly higher success rates in clinical development. Osteoporosis (OP) represents a major global health burden; however, the causal plasma proteome underlying OP remains largely unexplored, limiting the discovery of effective circulating biomarkers and therapeutic agents. - Source: PubMed
Publication date: 2026/08/08
Wang ZhenChen SixuLuo JunjieLiu ZhengboWen JingFeng BinyangYe Wen-HaoMa Jian-ChaoChen ZhenyueLi ZhenYang ZhenwenQiu JunxiangCui Zhong-Kai - Oral cancer (OC) remains a therapeutic challenge due to limited validated targets. Cis-pQTLs from the deCODE cohort (n = 35,559) were harmonized with OC-GWAS (3547 cases and 691,466 controls) meta-data through a two-sample Mendelian randomization (MR) framework. Robust Validation included replication in the UKB-PPP dataset, colocalization analysis, SMR (Summary-based MR), HEIDI (Heterogeneity in Dependent Instruments) tests, and eQTL evidence. Additional analyses encompassed protein-protein interaction (PPI) networks, Kyoto Encyclopedia of Genes and Genomes annotation (KEGG)/Gene Ontology (GO) pathway enrichment, mediation, Druggability and side effects analysis. Oral cancer (OC) remains a therapeutic challenge due to limited validated targets. Cis-pQTLs from the deCODE cohort (n = 35,559) were harmonized with OC-GWAS (3547 cases and 691,466 controls) meta-data through a two-sample Mendelian randomization (MR) framework. Robust Validation included replication in the UKB-PPP dataset, colocalization analysis, SMR (Summary-based MR), HEIDI (Heterogeneity in Dependent Instruments) tests, and eQTL evidence. Additional analyses encompassed protein-protein interaction (PPI) networks, Kyoto Encyclopedia of Genes and Genomes annotation (KEGG)/Gene Ontology (GO) pathway enrichment, mediation, Druggability and side effects analysis. To experimentally corroborate the MR findings, the quantitative real-time PCR (qRT-PCR) was performed to examine the mRNA expression levels of selected genes in oral squamous cell carcinoma (OSCC) cell lines (SCC-9 and SCC-25) and normal human oral epithelial cells (HOEC). Multi-omics MR identified TNFSF8 (p = 2.49 × 10, OR = 1.24) as a Tier 1 target. XXYLT1 (p = 1.41 × 10, OR = 1.34) and HSD17B14 (p = 0.04, OR = 2.00) achieved Tier 2. eQTLs-pQTLs Relationship revealed XXYLT1 expression explained 24.65% of risk through elevated plasma protein levels, TNFSF8 eQTLs mediated 72.80% via protein upregulation. Mediation analyses on CD4 on HLA DR+ CD4+ T cells (7.18%) contributed to the risk of OC by upregulating plasma HSD17B14, while daily cigarette consumption (20.63%) and CD8+ T cell percentage leukocytes (12.06%) contributed to the risk of OC by upregulating plasma TNFSF8. Drug safety assessments highlighted systemic TNFSF8 inhibition may elevate skin cancer risk. Multi-omics MR prioritizes TNFSF8 as a therapeutic target for oral cancer. Multi-omics MR identified TNFSF8 (p = 2.49 × 10, OR = 1.24) as a Tier 1 target. XXYLT1 (p = 1.41 × 10, OR = 1.34) and HSD17B14 (p = 0.04, OR = 2.00) achieved Tier 2. eQTLs-pQTLs Relationship revealed XXYLT1 expression explained 24.65% of risk through elevated plasma protein levels, TNFSF8 eQTLs mediated 72.80% via protein upregulation. Mediation analyses on CD4 on HLA DR+ CD4+ T cells (7.18%) contributed to the risk of OC by upregulating plasma HSD17B14, while daily cigarette consumption (20.63%) and CD8+ T cell percentage leukocytes (12.06%) contributed to the risk of OC by upregulating plasma TNFSF8. Drug safety assessments highlighted systemic TNFSF8 inhibition may elevate skin cancer risk. qRT-PCR confirmed significant upregulation of XXYLT1 and HSD17B14 in both SCC-9 and SCC-25 cell lines (p < 0.001), which is consistent with MR predictions. TNFSF8 was not reliably detected in these cancer cells, aligning with its proposed immune-mediated mechanism. Multi-omics MR prioritizes TNFSF8 as a therapeutic target for oral cancer. qPCR validation confirms the dysregulation of XXYLT1 and HSD17B14, while findings regarding TNFSF8 underscore its immune origin. These findings warrant further functional studies. - Source: PubMed
Huang MeishanWang HongweiMo XiaoqiangHuang XiongLiang TaoMo XiuwenLi MinsiFu RongLong XidaiHuang Xuanping - We and others have described homeostatic dysregulation of the CD4+ memory T-cell compartment with age. To gain greater insights into this dysregulation, we performed comprehensive single-cell genomic analysis of endogenous memory CD4+ T cells from young and aged mice. This analysis revealed 16 populations, composed of Th1, Th17, several subsets of regulatory T (Treg) cells, memory T cells, CD4+ CTLs, and T follicular helper (Tfh) cells. One of the most highly expressed genes in aged Tfh cells was Tnfsf8 (CD153 or CD30L), and flow cytometric analysis confirmed age-increased expression of CD153 on endogenous Tfh subsets and memory cells, but not Treg cells. At steady state, the absence of IL-6 significantly reduced CD153 expression on Tfh cells, and pharmacologic inhibition of c-MAF prevented IL-6-driven increase in CD153 expression. After immunization, expression of CD153 on Ag-specific CD4+ Tfh cells persisted significantly longer in aged mice, which required IL-6. Blockade of CD153 significantly reduced Tfh cell expression of ICOS and Ag-specific B-cell responses. Thus, although Tfh-mediated B cell responses, overall, normally decline with age, our data suggest that elevated expression of CD153, driven by an IL-6/c-MAF circuit, potentiates remaining Tfh function in aged mice. - Source: PubMed
Thomas Alyssa LWayman Joseph AAlmanan MahaFerguson AutumnBejjani Anthony TMiraldi Emily RChougnet Claire AHildeman David A