JDP2 antibody - N-terminal region (ARP31546_P050)
- Known as:
- JDP2 (anti-) - N-terminal region (ARP31546_P050)
- Catalog number:
- arp31546_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- JDP2 antibody - N-terminal region (ARP31546_P050)
Related genes to: JDP2 antibody - N-terminal region (ARP31546_P050)
- Gene:
- JDP2 NIH gene
- Name:
- Jun dimerization protein 2
- Previous symbol:
- JUNDM2
- Synonyms:
- -
- Chromosome:
- 14q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2008-03-26
- Date modifiied:
- 2017-03-10
Related products to: JDP2 antibody - N-terminal region (ARP31546_P050)
Related articles to: JDP2 antibody - N-terminal region (ARP31546_P050)
- Intratumoral heterogeneity (ITH) has been investigated primarily in locally advanced or metastatic cancer; however, much less is known about ITH in early-stage cancer, and the origins of ITH are poorly understood. Through single-cell and spatial transcriptomics of early-stage ground-glass opacity (GGO)-like lung adenocarcinoma (LUAD) (14 patients; 103,375 cells), we systematically define tumor states and demonstrate that pervasive transcriptional ITH exists in early-stage LUAD. Lineage diversification through epithelial plasticity, via a shift to less differentiated states and transdifferentiation, underlies a critical dimension of early ITH in lung cancer. We further reveal that decreased differentiation serves as a pathognomonic feature of malignant transformation and predicts poor prognosis. Notably, we identified a unique transitional state during AT2-to-AT1 transdifferentiation with activated tumor-suppressive pathways/genes. Integrative analysis of scRNA-seq, CUT&Tag, and bulk RNA-seq reveals that KLF4 and JDP2 are key transcription factors that reprogram LUAD into transitional state and inhibit progression. These findings elucidate ITH mechanisms in early-stage cancer and propose epithelial plasticity-targeted therapies. - Source: PubMed
Publication date: 2026/03/06
Xiong YangjieWang XiaofangYan KaiXin NingLi WeiqingZhang ZhengweiCheng YumeiZeng ChunlingLuo YuxiangLiu XiaoxiaoLu XiaojingYan XinhuiLan HaoqiWu TanwenDong YueLin XuLi YingJia XiaonaWang SiminTang HuaWang Yuexiang - Dysregulated immune responses often accompany severe COVID-19, but the underlying epigenetic mechanisms driving monocyte heterogeneity and COVID-19 progression remain unclear. Here, we applied single-cell multi-omics profiling to peripheral blood mononuclear cells across healthy and four COVID-19 severity stages. We identified two severity-associated classical monocyte subtypes-IL7R+ and CD163+, These subtypes exhibit distinct transcriptional and epigenetic landscapes. By constructing a gene regulatory network and perturbations, we revealed that ETS1 is a key driver of IL7R + monocytes with T cell-like signaling features and that JDP2 is a repressor that maintains the profibrotic, anti-inflammatory identity of CD163+ monocytes by suppressing AP-1 activity. These subtypes were enriched in the moderate-to-critical stages and exhibited signaling pathways associated with tissue remodeling and immune suppression. Our findings define monocyte heterogeneity as linked to COVID-19 severity and identify ETS1 and JDP2 as central regulators, offering insights into immune dysregulation, potential therapeutic targets for fibrosis, and long-term sequelae. - Source: PubMed
Publication date: 2026/01/29
Kim DonggunChoi Sin YoungKim Chae YeonYoo Jeong RaeKim Eui TaePark Jihwan - CD8 T cells differentiate into diverse states that shape immune outcomes in cancer and chronic infection. To define systematically the transcription factors (TFs) driving these states, we built a comprehensive atlas integrating transcriptional and epigenetic data across nine CD8 T cell states and inferred TF activity profiles. Our analysis catalogued TF activity fingerprints, uncovering regulatory mechanisms governing selective cell state differentiation. Leveraging this platform, we focused on two transcriptionally similar but functionally opposing states that are critical in tumour and viral contexts: terminally exhausted T (TEX) cells, which are dysfunctional, and tissue-resident memory T (T) cells, which are protective. Global TF community analysis revealed distinct biological pathways and TF-driven networks underlying protective versus dysfunctional states. Through in vivo CRISPR screening integrated with single-cell RNA sequencing (in vivo Perturb-seq) we delineated several TFs that selectively govern TEX cell differentiation. We also identified HIC1 and GFI1 as shared regulators of TEX and T cell differentiation and KLF6 as a unique regulator of T cells. We discovered new TEX-selective TFs, including ZSCAN20 and JDP2, with no previous known function in T cells. Targeted deletion of these TFs enhanced tumour control and synergized with immune checkpoint blockade but did not interfere with T cell formation. Consistently, their depletion in human T cells reduces the expression of inhibitory receptors and improves effector function. By decoupling exhaustion T-selective from protective T cell programmes, our platform enables more precise engineering of T cell states, accelerating the rational design of more effective cellular immunotherapies. - Source: PubMed
Publication date: 2026/02/04
Chung H KayLiu CongBattu AnamikaJambor Alexander NPratt Brandon MXie FucongRiesenberg Brian PCasillas EduardoSun MingLandoni ElisaLi YanpeiYe QidangJoo DanielGreen JarredSyed ZaidBrown Nolan JSmith MatthewMa ShixinTan ShirongChick BrentTripple VictoriaWang Z AudreyWang JunMcdonald BryanHe PeixiangYang QiyuanChen TimothyVaranasi Siva KarthikLaPorta Michael AMann Thomas HChen DanHoffmann FilipeHo JosephineModliszewski JenniferWilliams AprilLiu YushaWang ZhenLiu JieyuanGao YimingHu ZhitingCho Ukrae HLiu LongweiWang YingxiaoHargreaves Diana CDotti GianpietroSavoldo BarbaraThaxton Jessica EMilner J JustinKaech Susan MWang Wei - The expression of NPTX2, a neuronal immediate early gene (IEG) essential for excitatory-inhibitory balance, is altered in the earliest stages of cognitive decline that anticipate Alzheimer's disease (AD). Here, we use NPTX2 as a point of reference for Omics studies to identify genes and pathways linked to its position in AD onset and progression. We integrated bulk RNA sequencing from 575 middle temporal gyrus (MTG) samples across four cohorts together with targeted proteomics in the same samples using parallel reaction monitoring-mass spectrometry in 135 representative cases, focusing on 20 curated proteins spanning synaptic, trafficking, lysosomal, and regulatory categories. NPTX2 RNA and protein were significantly reduced in AD, and to a lesser extent in mild cognitive impairment (MCI) samples. BDNF, VGF, SST, and SCG2 correlated with both NPTX2 mRNA and protein. We identified NPTX2 correlated synaptic and mitochondrial programs that were negatively correlated with lysosomal and chromatin/stress modules. Gene set enrichment analysis (GSEA) of NPTX2 correlations across all samples confirmed broad alignment with synaptic and mitochondrial compartments, while more NPTX2-specific associations were observed with proteostasis and translation regulator pathways, which were weakened in AD. In contrast, correlation of NPTX2 protein with transcriptomic profiles revealed negative associations with stress-linked transcription regulator RNAs (FOXJ1, ZHX3, SMAD5, JDP2, ZIC4), which were strengthened in AD. Studies position NPTX2 as a hub of an activity-regulated "plasticity cluster" (BDNF, VGF, SST, SCG2) that encompasses interneuron function and is embedded on a neuronal/mitochondrial integrity axis that is inversely coupled to lysosomal/chromatin-stress programs. In AD, these transcript-level correlations broadly weaken, and stress-linked transcriptional regulators become more prominent, suggesting a role in NPTX2 loss of function. - Source: PubMed
Publication date: 2025/10/20
Lao YuelinXiao Mei-FangJi ShiyuPiras Ignazio SBonfitto AnnaSong SerenaAldabergenova ArailymNa Chan-HyunSloan JenniferTrejo AdrielGeula ChangizRogalski Emily JKawas Claudia HCorrada Maria MSerrano Geidy EBeach Thomas GTroncoso Juan CHuentelman Matthew JBarnes Carol AWorley Paul FColantuoni Carlo - All jawed vertebrates have a highly coordinated innate immune response to viral infections driven by a core set of interferon responsive genes (ISGs), but interspecies variation remains substantial. In this study, we examined the genome-wide regulatory basis for antiviral gene expression responses in Atlantic salmon (), representing a teleost family that underwent a whole genome duplication (WGD) event ~100 Mya. We stimulate fish systemically with polyinosinic:polycytidylic acid (poly I:C), a synthetic viral mimic, and profile transcriptomic and epigenomic responses in the primary hematopoietic and lymphoid tissue. We used ATAC-seq and ChIP-seq (H3K27ac and H3K27me3), combined with mRNA-seq, to comprehensively examine modifications in gene regulation following stimulation. We identified a set of 197 ISGs with regulatory elements showing increased chromatin accessibility and H3K27ac signal in concert with increased gene expression in response to poly I:C. Fifty-four of these genes were conserved ISGs in rainbow trout, zebrafish, and human. Our analysis provides evidence for conserved transcription factors (TFs) driving the interferon response by binding ISG promoters, including IRF8, IRF9, STAT1, and STAT2. Regulatory elements within differentially expressed genes were enriched for predicted binding sites for STAT6, PRDM1, IRF6, JDP2, NR2E1, and BCL6, suggesting a central role for these TFs in the antiviral response. Finally, we demonstrate paralog-specific enrichment of interferon-stimulated response element (ISRE) motifs in poly I:C activated promoters of ISGs retained as duplicates from the salmonid WGD. Overall, this study provides novel insights into the genomic regulatory landscape underlying antiviral immunity in a farmed fish with a complex genome. - Source: PubMed
Publication date: 2025/10/22
Naseer ShahmirClark Thomas CCollet BertrandDewari PooranBaranasic DamirMacqueen Daniel JBoudinot PierreMartin Samuel A M