JUNB
- Known as:
- JUNB
- Catalog number:
- Y214315
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- JUNB
Related genes to: JUNB
- Gene:
- JUNB NIH gene
- Name:
- JunB proto-oncogene, AP-1 transcription factor subunit
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19p13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2016-05-03
Related products to: JUNB
Related articles to: JUNB
- Ovarian carcinoma is a difficult-to-treat cancer. It is often resistant to chemotherapy and targeted therapy. The 5-year survival rates of patients with advanced tumors are usually below 40%. Immunotherapy represents an emerging treatment option. We investigated the prognostic significance of the oncogenic transcription factor AP-1, formed by the dimerization of FOS and JUN family members. - Source: PubMed
Dawood MonaOoko EdnahEfferth ThomasBoulos Joelle C - - Source: PubMed
Publication date: 2026/04/27
Mei HaonanNi XinmiaoZheng QingyuanTang HaoYan ZhiweiYang SongXiong YufengHui YuminJian JunWang JingsongYang XiangxiangLiu XiuhengChen Zhiyuan - Transforming growth factor β (TGF-β) signaling is a highly pleiotropic pathway with an important role in development, homeostasis, and cancer. Chromatin regulators contribute to the regulation of TGF-β-responsive transcription. The requirement of subunits of the MLL3/MLL4 histone methyltransferase complexes for TGF-β responses has been reported. However, their exact roles are not fully understood. To investigate the functions of these complexes, we employed CRISPR/Cas9 genome editing to inactivate the or genes in human diploid epithelial cells. Time-course RNA-seq experiments revealed the requirement of MLL4 but not of MLL3 for TGF-β transcriptional responses. CUT&RUN experiments showed that MLL4 binding increases after TGF-β treatment and is especially enriched at AP-1 transcription factor binding sites. Interestingly, TGF-β-induced chromatin binding of MLL4 correlates with increases in H3K27ac but not in H3K4me1 modifications. Furthermore, TGF-β treatment sets off SMAD2-induced JUNB expression, which forms a feed-forward loop with MLL4. By inhibiting the activities of AP-1, the BAF chromatin remodeler, or the CBP/p300 histone acetyltransferase, we found that AP-1 binding and these chromatin regulators are all necessary for TGF-β induction of MLL4 binding and transcriptional activation of its genomic targets. Taken together, our study reveals distinctive roles for the MLL3 and MLL4 paralogs in the transcriptional response to TGF-β. In contrast to MLL3, MLL4 forms a feed-forward loop of JUNB, the BAF complex, and CBP/p300 to sustain transcription activation by TGF-β. - Source: PubMed
Publication date: 2026/04/24
Chan Timothy En HawIslam Md SaifulFotouhi OmidBozkurt MertNizamuddin SheikhSchüle Katrin MArnold Sebastian JTimmers H T Marc - The liver has a unique capacity for self-renewal, maintaining a proper liver-to-bodyweight ratio, which is essential for sustaining homeostasis. Regenerative process in the liver involves intricate communication between various cell types such as hepatocytes, hepatic stellate cells, endothelial cells, and inflammatory cells. Although the role of endothelial cells in liver regeneration has been extensively studied, detailed knowledge regarding specific endothelial cell-derived factors that promote the regeneration of liver endothelial cells (LECs) remains limited. This study aimed to identify the regenerative capacity of endothelial progenitor cells (EPCs) after acute liver injury. - Source: PubMed
Publication date: 2026/03/28
Lee Jong-MinHa Yoon-SuLee Seung-JunKim Hyun-YiAdpaikar Anish AshokKim Eun-JungOtsu KeishiChe XiangguoHan Dai HoonHer YoungChoi Je-YongKim Seung-JinJung Han-Sung - Epigenetic enzymes, writers, readers and erasers regulate chromatin landscapes and participate in tumor heterogeneity. While therapeutic targeting of these enzymes has shown clinical promise, the comparative efficacy of mono-versus dual-inhibitor strategies remain unclear. Here, we introduce a multi-modal platform that uses NicE-viewSeq and integrates automated deep learning based spatially resolved chromatin accessibility profiling with high-throughput sequencing following epigenetic inhibitor application. Accessible chromatin landscapes were altered along with nucleosome positioning following inhibition of either LSD1 or HDACs alone, or both together. Coordinated modulation of histone marks and the CoREST complex on chromatin was observed across inhibitory conditions. Transcription factor binding analysis identified three predominant families, ETS, RUNT, and bZIP with enhanced chromatin association upon treatments. Mechanistically, a CoREST-RUNX regulatory axis was uncovered wherein JunB, a member of bZIP family displaces CoREST-RUNX at differentially accessible regions, triggering apoptotic pathways. Therefore, JunB-mediated mechanism reveals a convergent therapeutic vulnerability, offering new avenues for optimizing different combinatorial epigenetic therapy in cancer. - Source: PubMed
Publication date: 2026/04/11
Sen SagnikEstève Pierre OTarasia DeveshDanneberg RachelDey AshmitaMaulik UjjwalBandyopadhyay SanghamitraPradhan Sriharsa