JunD (Phospho_Ser255) Antibody
- Known as:
- JunD (Phospho_Ser255) Antibody
- Catalog number:
- E011028-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- JunD (Phospho_Ser255) Antibody
Related genes to: JunD (Phospho_Ser255) Antibody
- Gene:
- JUND NIH gene
- Name:
- JunD proto-oncogene, AP-1 transcription factor subunit
- Previous symbol:
- -
- Synonyms:
- AP-1
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2016-10-11
Related products to: JunD (Phospho_Ser255) Antibody
Related articles to: JunD (Phospho_Ser255) Antibody
- Classic hairy cell leukemia (HCL) is a rare indolent B cell lymphoproliferative disorder characterized by the driver mutation BRAF V600E. Standard treatment with purine analogs (i.e. cladribine) induces long-term remissions, but up to 25% of patients relapse early. Even when targeting BRAF V600E, residual HCL cells frequently persist in the bone marrow (BM). To unravel additional biologic alterations contributing to HCL disease persistence, we performed single-cell RNA sequencing in sorted primary HCL cells from long-term versus short-term cladribine responders (LT-R versus ST-R: >10 versus ≤3 years PFS) at diagnosis and in ST-R at diagnosis versus relapses. We identified a distinct HCL subcluster characterized by elevated DUSP1, FOS, and JUND expression, which was detected in all patients and persisted or even expanded at relapses. Cancer pathway analysis suggested enhanced tumor microenvironment dependency as reflected by suppression of the p38-MAP kinase pathway. In the absence of a suitable BRAF V600E-mutated HCL cell line, we validated HAIR-M cells (BRAF D594E) as a bona fide experimental HCL model. The activating BRAF D594E mutation mimics V600E-induced downstream signals that can efficiently be targeted by BRAF inhibitors (BRAFi). HAIR-M co-culture with BM stromal cells (BMSC) strongly induced DUSP1 that was accompanied by protection from BRAFi-induced HAIR-M apoptosis. The functional importance of DUSP1 was corroborated by demonstrating that BMSC-induced protection from cell death could be overcome through DUSP1 inhibition. Our results might set the stage for future clinical testing of DUSP1 inhibition to eliminate minimal residual disease (MRD) and prevent disease relapse in HCL. - Source: PubMed
Publication date: 2026/05/27
Bohn Jan-PaulScheiber AlexandraSturm GregorMaurer ThomasMair AnnaKugler ValentinaFeichtner AndreasFritz AlexandraTorres-Quesada OmarJaeger UlrichHuber Roland GDaum SophiaMartowicz AgnieszkaRedlinger NorbertPircher AndreasSopper SieghartTrajanoski ZlatkoStefan EduardSalcher StefanWolf Dominik - Dysregulated stress responses are increasingly implicated in the pathophysiology of autism spectrum disorder (ASD). Astrocytes, which are highly vulnerable to stress, critically support neuronal survival; however, their specific role in ASD remains poorly defined. - Source: PubMed
Publication date: 2026/05/19
Wang QiYin HuaminJiang QiQi YuboBai JieliWang ZhendongLiu KailaiSun RuizhenWang WenhangLiu CanyingYan WeishuoLuo JinDuan LianShan Zhiyan - Endometriosis (EMs) is a common gynecological disorder characterized by ectopic endometrial tissue growth, leading to chronic inflammation and pelvic pain. Despite its high prevalence, the molecular mechanisms underlying EMs remain poorly understood. This study aims to identify key biomarkers and elucidate the role of ferroptosis in EMs pathogenesis. - Source: PubMed
Publication date: 2026/05/18
Yang YuanHuang YiWang YidanLi RuiyunLi Hongrui - Immune checkpoint blockade has shown benefit in some Triple-negative breast cancer (TNBC) patients, but responses are variable. BRCA1-mutated TNBC represents a biologically distinct subgroup, potentially differing in immunogenicity and immunotherapy responsiveness. However, immune microenvironment differences between BRCA1-mutated and sporadic TNBC remain incompletely understood. By performing single-cell RNA sequencing analysis on sporadic TNBC and BRCA1 mutant TNBC, we assessed immune cell composition, transcriptional program, pathways, stemness, differentiation, and transcription factor regulatory networks. B cell and plasma cell subtypes were further explored using AUCell, CytoTRACE, Monocle2, and Slingshot. Compared to sporadic TNBC, BRCA1-mutated TNBC exhibited a distinct immune landscape with enriched naïve and memory B cells, while sporadic TNBC was dominated by terminally differentiated plasma cells, including IgA plasma cells. Functional enrichment analyses showed enhanced adaptive immune signaling, antigen presentation, and B cell receptor pathways in BRCA1-mutated TNBC, while sporadic TNBC had humoral effector and immunoregulatory programs. Trajectory and stemness analyses indicated enhanced cellular plasticity and decreased differentiation in B cells derived from BRCA1-mutated triple-negative breast cancer. Analysis of transcription factors revealed JUND and ETV1 in BRCA1-mutated TNBC, and MEIS1 and CEBPB in sporadic TNBC. Our findings underscore disparities in the immune ecosystem between BRCA1-mutated and spontaneous TNBC, indicating that the B cell-centric immunological milieu in BRCA1-mutated TNBC may offer a more advantageous setting for immunotherapy. Sporadic TNBC, by contrast, exhibits an immunological state characterized by plasma cells, which may restrict immune reactivation. These data indicate that B cell-based immunological stratification may guide precision immunotherapy approaches. - Source: PubMed
Publication date: 2026/05/12
Sun QiZhong YutingSun Changgang - The mechanisms underlying gastric cancer (GC) progression, including recurrence and metastasis, remain unclear. Studies have reported that microRNAs and Men1 are closely associated with multiple tumors, including GC. Therefore, assessing the impact of Men1 on GC and investigating the underlying mechanisms are essential. - Source: PubMed
Publication date: 2026/05/06
Jiang Jin-XunZhang Shi-JieZhao KunZheng Kai-TianWang Shan-HuChen Tian-deWang Zhen