FN14 Polyclonal Antibody [AT112]
- Known as:
- FN14 Polyclonal Antibody [AT112]
- Catalog number:
- A-0501-100
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- EpigenTek
- Gene target:
- FN14 Polyclonal Antibody [AT112]
Related genes to: FN14 Polyclonal Antibody [AT112]
- Gene:
- TNFRSF12A NIH gene
- Name:
- TNF receptor superfamily member 12A
- Previous symbol:
- -
- Synonyms:
- FN14, TweakR, CD266
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-20
- Date modifiied:
- 2016-06-28
Related products to: FN14 Polyclonal Antibody [AT112]
Related articles to: FN14 Polyclonal Antibody [AT112]
- Keratinocytes play a central role in amplifying skin inflammation in psoriasis and atopic dermatitis (AD). However, the epithelial-intrinsic regulators involved in responsiveness to inflammatory cues remain poorly defined. MiRNAs are fundamental regulators of gene expression. - Source: PubMed
Publication date: 2026/06/26
Luo LonglongYuan HaoSrivastava AnkitAnnusver KarlKhera NupurSaha PiyalPrieux RoxaneMahapatra Kunal DasKelemen EvelynDholakia MenilFreisenhausen Jan CedricPetkova MilenaAgerberg KlasDompage Devin MalithaMäkinen TaijaFyhrquist NannaPejler GunnarKasper MariaPivarcsi AndorSonkoly Enikö - This study aimed to comprehensively analyze differentially expressed genes (DEGs) in chondrocytes from patients with knee osteoarthritis (OA) by integrating multiple machine learning algorithms and bioinformatics techniques, to unravel the underlying molecular mechanisms associated with OA chondrocytes, and to provide novel insights for the innovation of clinical therapeutic strategies. - Source: PubMed
Publication date: 2026/06/16
Zhuge Jing-leLi Xi-YongWang Yong-leMa Juan-Fen - 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 - Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide, with metastasis representing a major determinant of poor prognosis. Epithelial-mesenchymal transition (EMT) promotes metastatic progression by enhancing tumor cell migration and invasion. This study aimed to identify EMT-associated malignant epithelial programs in CRC and define the macrophage-tumor cell signaling mechanisms contributing to EMT and apoptosis resistance. We integrated single-cell RNA sequencing, bulk RNA-seq, spatial transcriptomics, immunohistochemistry, and functional validation experiments. Malignant epithelial subpopulations were identified using inferCNV and reclustering analyses, and EMT-related programs were evaluated by gene set scoring. Transcriptional regulation was assessed using pySCENIC, public ChIP-seq data, ChIP-qPCR, and TNFRSF12A promoter luciferase reporter assays. Cell-cell communication and ligand activity were analyzed using CellPhoneDB and NicheNet. Functional validation included western blotting, conditioned-medium assays, TNFSF12 neutralization, and Transwell migration assays. We identified an EMT-associated malignant epithelial subgroup enriched for TNFRSF12A expression. FOSL2 was highly active in this subgroup and positively associated with TNFRSF12A expression. ChIP-qPCR and promoter luciferase assays supported direct FOSL2-mediated transcriptional activation of TNFRSF12A. APOE+ macrophages were identified as a potential source of TNFSF12 in the tumor microenvironment. TNFSF12 acted on TNFRSF12A-expressing CRC cells and was associated with BCL2L1 upregulation, EMT-like changes, and enhanced migration. TNFSF12 overexpression increased BCL2L1 expression, whereas APOE+ macrophage-conditioned medium promoted E-cadherin downregulation, Vimentin and BCL2L1 upregulation, and tumor cell migration. These effects were attenuated by anti-TNFSF12 neutralization. Clinically, combined high TNFSF12 and TNFRSF12A expression was associated with advanced disease stage and poorer survival. Together, these findings identify a macrophage-tumor cell signaling axis in which FOSL2 upregulates TNFRSF12A in CRC cells, while APOE+ macrophage-derived TNFSF12 activates downstream BCL2L1-associated survival and EMT-related programs. The TNFSF12-TNFRSF12A-BCL2L1 pathway may represent a potential therapeutic vulnerability in metastatic CRC. NOVELTY AND IMPACT: This study identifies a previously undercharacterized macrophage-tumor cell signaling mechanism in colorectal cancer (CRC), in which APOE+ macrophage-derived TNFSF12 acts on TNFRSF12A-expressing malignant epithelial cells to promote EMT-associated progression. By integrating single-cell transcriptomics, bulk RNA-seq, spatial transcriptomics, and functional validation, we show that FOSL2 directly enhances TNFRSF12A transcription in EMT-associated tumor cells, thereby increasing their responsiveness to TNFSF12. Functionally, TNFSF12/TNFRSF12A signaling promotes BCL2L1-associated survival signaling, EMT-like changes, and tumor cell migration, while combined high TNFSF12 and TNFRSF12A expression is associated with advanced disease stage and poor patient survival. These findings reveal a clinically relevant macrophage-tumor cell communication axis and highlight the TNFSF12-TNFRSF12A-BCL2L1 pathway as a potential therapeutic vulnerability in metastatic CRC. - Source: PubMed
Publication date: 2026/05/20
Song ChuanjunSun HongyuGan WenyuanLiu QuanzhongWu LingxiangZhu MengyanZhu Lingjun - Carpal tunnel syndrome (CTS) is an entrapment neuropathy resulting from compression of the median nerve at the wrist level. The aim of the study was to investigate the efficacy of tumor necrosis factor-like weak apoptosis inducer (TWEAK) and its receptor, inducible fibroblast growth factor 14 (Fn14) axis in CTS and to conduct a preliminary study on the usability of TWEAK/Fn14 as a new pharmacological treatment target in CTS. - Source: PubMed
Publication date: 2026/04/22
Yevgi RecepŞimşek FatmaLaloğlu Esra