IL12A _ NKSF1 Antibody
- Known as:
- IL12A _ NKSF1 Antibody
- Catalog number:
- 10021-RP01
- Product Quantity:
- 200
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- IL12A _ NKSF1 Antibody
Related genes to: IL12A _ NKSF1 Antibody
- Gene:
- IL12A NIH gene
- Name:
- interleukin 12A
- Previous symbol:
- NKSF1
- Synonyms:
- CLMF, IL-12A, p35, NFSK
- Chromosome:
- 3q25.33
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-08
- Date modifiied:
- 2014-11-18
Related products to: IL12A _ NKSF1 Antibody
Related articles to: IL12A _ NKSF1 Antibody
- Pterygium is a common ocular surface disorder with multifactorial etiology involving environmental exposure and immune dysregulation. Interleukin-12 (IL-12), a key immunomodulatory cytokine, has been implicated in inflammation and tumor-related processes, yet its genetic contribution to pterygium remains unclear. This study aimed to evaluate the association between polymorphisms and pterygium susceptibility. - Source: PubMed
Yang Ya-ChenHsia Ning-YiHsia Te-ChunHu Pei-ShinChang Wen-ShinTsai Chia-WenBau DA-Tian - The present study aimed to characterize the immune response, differential gene expression, and functional alterations observed following an in vivo challenge of Classical Swine Fever Virus (CSFV) in crossbred pigs. RNA-sequencing was performed on whole blood samples collected from three pigs before and at 7 days post-infection. A total of 3428 differentially expressed genes (DEGs) were identified, including 970 significantly upregulated and 261 downregulated genes (|log fold change| ≥ 1.5, adjusted p < 0.05). The most prominent DEG was LAMB4, a gene associated with cellular attachment receptors facilitating CSFV binding to porcine cells. Several cytokine-cytokine receptor interaction genes, such as CXCL12, CCL2, CCR1, and IL10RA, were upregulated, indicating a strong activation of innate immune responses. Simultaneously, multiple adaptive immune genes, including CD28, CD83, SLA-DQB1, and IL1A, IL12A, IL26 were downregulated, suggesting viral-mediated suppression of antigen presentation and T-cell signaling. Pathway analysis highlighted the involvement of platelet activation and coagulation cascades during viral evasion. Protein-protein interaction (PPI) analysis revealed a core antiviral module comprising MX1, MX2, ISG15, IFIH1, OASL, IFIT1, and UBE2L6, which are central to interferon signaling and viral restriction. Transcription factors such as ETV7, TOX3, and MSC were upregulated, pointing to immune modulation and possible T-cell exhaustion. Conversely, downregulation of HES1, PRDM6, and MYOG indicated impaired lymphocyte differentiation and tissue repair. Overall, the findings suggest a dual host response to CSFV, with strong innate activation alongside adaptive immune suppression, providing valuable insights for vaccine and therapeutic development. - Source: PubMed
Publication date: 2026/06/25
Singh AyushiKumar AmitKhanna ShivaniDhar PronabLatheef Shyma KUpmanyu VikramadityaAgrawal Ravi KantYadav Ajay KumarUpadhyay AmritanshuChand Devatwal PremDwivedi ShraddhaDutt Triveni - Enhancing innate-adaptive immune crosstalk is key for improving cancer vaccine efficacy. TRIMELVax is a heat shock-conditioned whole-tumor-cell vaccine combining xenogeneic melanoma cell lysate, syngeneic B16F10 melanoma cell lysate, and hemocyanin. Although TRIMELVax elicits robust antitumor responses in preclinical models, the mechanisms underlying its efficacy remain poorly defined. We characterized the early immune events triggered by TRIMELVax in mice using RT-qPCR, high-dimensional flow cytometry, immunohistochemistry, CFSE-based dendritic cell (DC) migration assays, and therapeutic melanoma models with transient neutrophil depletion. TRIMELVax elicited a rapid inflammatory response at the vaccination site, characterized by local upregulation of , and . This response drove an early influx of neutrophils and monocytes, followed by increased accumulation of cDC1, cDC2, and monocyte-derived DCs. Notably, we identified a transient population of neutrophils expressing markers associated with antigen-presenting cells (CD45⁺, CD11b⁺, Ly6G⁺, CD11c⁺, MHC-II⁺) that emerged within 12-24 hours postvaccination. These APC-like neutrophils colocalized with cDC1 at the injection site and subsequently migrated to the popliteal draining lymph nodes (pLN). Neutrophil depletion impaired cDC1 migration, reduced APC accumulation in pLN, and abolished the therapeutic efficacy of TRIMELVax. Together, these findings identify neutrophils as key early regulators of the innate inflammatory environment induced by TRIMELVax and suggest that neutrophils with APC-like features may impact DC trafficking and downstream antitumor immunity. Neutrophils, particularly those with APC-like phenotypes, emerge as promising cellular adjuvant targets for enhancing cancer vaccination strategies, offering a new avenue for rational vaccine design and combination with checkpoint blockade therapies. - Source: PubMed
Publication date: 2026/06/25
Pérez-Baños AmarilisGleisner María AlejandraTittarelli AndrésTapia DanielaCuevas María ElisaMardonez AntoniaTempio FabiánAstaburuaga-García RosarioFlores IvánPereda CristianLladser ÁlvaroGonzález Fermín EValenzuela SebastiánRicca MicaelaBecker María InésBlüthgen NilsAchour AdnaneSalazar-Onfray Flavio - Hepatocellular carcinoma (HCC), the most common primary liver cancer, exhibits metabolic reprogramming with disrupted cholesterol metabolism as a key feature. Lecithin-cholesterol acyltransferase (LCAT) contributes to HCC development, but its exact on cogenic mechanisms remain unclear. This study aims to investigate the role of LCAT in hepatocarcinogenesis and elucidate its underlying molecular mechanisms in HCC. - Source: PubMed
Publication date: 2026/06/15
Gao HongliangPeng XingWen YaliGou LimingXu YanchaoQu XuanWu JingXue Bin - Porokeratosis (PK) encompasses genetically heterogeneous keratinization disorders, with disseminated superficial actinic porokeratosis (DSAP) and porokeratosis ptychotropica (PPt) as distinct subtypes. Although MVK is a known causative gene, how different variants drive distinct phenotypes remains unclear. Through whole-exome sequencing of two DSAP patients, we identified an MVK variant (c.439G > A, p.Ala147Thr) cataloged as likely pathogenic in ClinVar yet uncharacterized functionally in DSAP keratinocytes. A previously reported PPt-associated variant (c.64G > A) was included for comparison. We established HaCaT cells stably overexpressing each mutant via lentiviral transduction and validated expression by qPCR and Western blot. Integrated transcriptomic and proteomic analyses identified differentially expressed genes (DEGs) and proteins (DEPs) across MVK439 versus control, MVK64 versus control, and MVK439 versus MVK64 groups, followed by GO and KEGG enrichment. Transcriptomic profiling revealed 231, 1,849, and 2,329 DEGs in the respective comparisons. Proteomic screening identified 2,673 DEPs, with 42 shared across all groups, 77 specifically associated with c.439G > A, and 832 linked to c.64G > A. Integrated analysis suggested IL12A and pIgR as potential contributors to c.439G > A-driven DSAP, while CXCL11, CXCL9, and TNFRSF12A may mediate c.64G > A-induced PPt. These findings offer new insights into MVK function and PK pathogenesis, warranting validation in larger cohorts. - Source: PubMed
Publication date: 2026/06/03
Lai ShuqinZhu WenjieLin ChunliGuo ZimengChen ShiqiXie LangLiu JieZeng ZhaolinYou CongLi Longnian