Mouse CD30L ELISA kit
- Known as:
- Mouse CD30L Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- LF-EK50557
- Product Quantity:
- 1×96T
- Category:
- Peptides
- Supplier:
- Abfron
- Gene target:
- Mouse CD30L ELISA kit
Related genes to: Mouse 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
Related products to: Mouse CD30L ELISA kit
Related articles to: Mouse CD30L ELISA kit
- 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 - M2 macrophages are closely associated with an immunosuppressive tumor microenvironment (TME) and may influence drug response, but their clinical relevance in osteosarcoma (OS) remains to be comprehensively elucidated. This study developed an M2-related model to predict the risk, immune response, and drug sensitivity for patients with OS. - Source: PubMed
Publication date: 2026/07/07
Chen HuihuangZhuang MinxianChen ShijieLin BeiXu DongminLin WentaoFeng EryouLin Dasheng - Multiple sclerosis (MS) is a complex immune-mediated disorder with polygenic and multicellular underpinnings, necessitating cell-type-specific molecular studies to delineate dysregulated pathways. Here, we profile 1,075 transcriptomes from 167 patients with MS and 42 healthy participants across six peripheral immune cell-type-states. MS-associated transcriptional differences are more pronounced in primary (unstimulated) immune cells than in in vitro-stimulated counterparts. We identify shared and cell-type-specific transcriptional alterations at the level of genes, pathways, and co-expressed gene modules, prioritizing regulators, such as ZBTB16, across T cells and monocytes, and replicating six MS-associated modules in independent datasets. The top T cell module is enriched for MS susceptibility genes and affects proliferation. The top monocyte module implicates dysregulated TNF-α/NF-κB signaling, for which an in silico drug screen and in vitro validation nominate alvespimycin as a candidate modulator. Together, these findings define stable peripheral immune dysregulation signatures in MS that may serve as diagnostic or prognostic biomarkers in at-risk individuals. - Source: PubMed
Publication date: 2026/06/06
Roostaei TinaFujita MasashiTouil HananeKivisäkk PiaMcCabe CristinNejad ParhamSabrin AfsanaGarcia Frankie Gvan Dorp Christiaan HFelsky DanielVlachos Ioannis SHui DanielFransson JenniferMacnair WillWilliams AnnaZhang LiliZhu WenXia ZongqiZujovic ViolettaPatsopoulos Nikolaos AYates Andrew JKuchroo Vijay KChitnis TanujaWeiner Howard LKlein Hans-UlrichDe Jager Philip L