JUNB antibody - N-terminal region (P100946_T100)
- Known as:
- JUNB (anti-) - N-terminal region (P100946_T100)
- Catalog number:
- p100946_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- JUNB antibody - N-terminal region (P100946_T100)
Related genes to: JUNB antibody - N-terminal region (P100946_T100)
- 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 antibody - N-terminal region (P100946_T100)
Related articles to: JUNB antibody - N-terminal region (P100946_T100)
- 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 - Temporomandibular joint osteoarthritis (TMJOA) is recognized as one of the most important oral-maxillofacial degenerative diseases, and affects a large group of the population worldwide. The progression of TMJOA is accompanied by an imbalance of cytokines in the joint cavity and a slow but long-lasting degradation of the joint tissues. FGF8, an important member of the fibroblast growth factor family, has been shown to be up-regulated in the cavities of osteoarthritis joints. However, its role in TMJOA progression remains unclear. Here, we established a mouse TMJOA model by using unilateral anterior crossbite (UAC), and investigated the role of FGF8 on the changes in condylar cartilage in the progress of TMJOA by using adeno-associated virus carrying FGF8 gene. We found that FGF8 accelerated the cartilage deterioration during TMJOA progression. FGF8 overexpression partially impaired the mature phenotype of chondrocytes by decreasing the expression of collagen type II (COL2A1) and aggrecan, and exacerbated chondrocyte hypertrophy by increasing the expression of collagen type X (COL10A1), matrix metallopeptidase 13 (MMP13) and a disintegrin and metalloproteinase with thrombospondin 5 (ADAMTS5). FGF8 promotes chondrocyte cytokine perturbation by up-regulating the expression profiles of inflammatory factors, chemotactic factors and interferons and down-regulating the expression of growth factors via the transcription factor JunB. Furthermore, FGF8-mediated JunB facilitates chondrocyte hypertrophy by binding to the promoters of Col10α1 and Mmp13. These results help understand the importance of FGF8 in the progression of TMJOA and provide cues for potential therapeutic strategies for osteoarthritis. - Source: PubMed
Publication date: 2026/04/14
Chen HaoranFeng ShuoLi ChengLiu YongtaoXue ChengXie JingZuo Tao - Familial thoracic aortic aneurysm and dissection (FTAAD), caused by the pathogenic Myh11 K1256del variant, is characterized by impaired aortic contractility; however, how reduced contractility predisposes the aorta to dissection remains incompletely understood. In this study, we performed a data-driven trans-omic upstream analysis using Genome Enhancer to identify key regulatory mechanisms in aortas from Myh11 K1256del mice under baseline conditions, without exposure to exogenous pathological stimuli. Transcriptome analysis revealed enrichment of genes related to smooth muscle contraction and regulation of myosin light chain phosphatase activity. Upstream computational analysis of regulatory regions identified nuclear factor of activated T cells 1 and lymphoid enhancer-binding factor 1 as major transcription factors, and further highlighted Rho-associated, coiled-coil-containing protein kinase 1 (ROCK1) as a predicted central regulator of the dysregulated transcriptional network. Druggability analysis suggested ROCK1 and the JunB proto-oncogene AP-1 transcription factor subunit as potential therapeutic targets. Furthermore, it predicted 51 candidate therapeutants, including atorvastatin, GSK-269962A, and atovaquone. These findings indicate that even in the absence of overt pathological stimulation, aortic tissue carrying the Myh11 K1256del variant exhibits a transcriptional program centered on ROCK signaling, which may prime the aorta for maladaptive responses to additional stress and may enhance susceptibility to dissection. This computational analysis requires experimental validation, but may provide a hypothesis-generating framework for development of preventive pharmacological interventions against FTAAD. - Source: PubMed
Publication date: 2026/03/31
Okuhata HironoriTomida ShotaIshima TamakiNagai RyozoAizawa Kenichi - Genetic background is a major determinant of disc degeneration, a leading cause of chronic back pain and disability. Herein, we demonstrate that premature disc cell senescence contributes to early-onset degeneration in SM/J mice and test two systemic senotherapeutic strategies to mitigate it: Navitoclax (Nav.) and a cocktail of Dasatinib and Quercetin (DQ). While Nav. treatment did not improve severe degeneration in SM/J mice or senescence status, DQ-treated mice showed lower grades of degeneration and a decreased abundance of senescence markers, including p19ARF, p21, and the senescence-associated secretory phenotype (SASP). DQ improved disc cell viability and phenotype retention and retarded fibrosis of the nucleus pulposus tissue. Transcriptomic analysis revealed tissue-specific effects of the treatment, with cell cycle regulation and JNK signaling being commonly affected across different tissue types. A comparison of SM/J data with DQ-mediated aging-dependent amelioration of disc degeneration in C57BL/6 N mice identified Junb and Zfp36l1 signaling as shared DQ targets in the mouse disc. Notably, the in vitro inhibition studies of the JUN pathway in human degenerated NP cells mimicked the benefits of DQ, namely, a reduction in senescence and SASP. This study reinforces the efficacy of senolytic treatment in ameliorating local senescence and intervertebral disc fibrosis. - Source: PubMed
Publication date: 2026/04/14
Novais Emanuel JOttone Olivia KJagannath SanjanaAkande Esther JesutofunmiBarve Ruteja ARisbud Makarand V - Allergic rhinitis (AR) is a chronic inflammatory disorder characterized by type 2 T helper (Th2) cell-dominant immune responses. NEDD4 like E3 ubiquitin protein ligase (NEDD4L) plays a role in regulating T cell activation and Th cell differentiation. Dipeptidyl peptidase 4 (DPP4) is involved in Th2 inflammatory responses in AR. In this study, NEDD4L was found to be downregulated in peripheral blood CD4-enriched T cells from AR patients. In a BALB/c mouse model of AR, established by intraperitoneal sensitization with 25 μg ovalbumin (OVA) followed by intranasal challenge with 500 μg OVA, NEDD4L expression was also reduced in splenic T cells enriched in CD4 populations. T cell-specific overexpression of NEDD4L, achieved via tail vein injection of lentivirus carrying the CD3δ promoter, significantly alleviated AR symptoms, as shown by reduced sneezing and nose-wiping frequency, and decreased serum levels of OVA-specific immunoglobulin E (IgE) and histamine. Moreover, NEDD4L overexpression attenuated nasal mucosal thickening, inflammatory cell infiltration, and goblet cell hyperplasia. In vitro, lentiviral-mediated NEDD4L overexpression in T cells, enriched in CD4 populations, is associated with suppression of Th2-linked inflammation, as indicated by decreased GATA-binding protein 3 (GATA-3) and JunB proto-oncogene (JunB) protein levels, reduced secretion of Th2 cytokines, and a lower proportion of CD4IL-4 cells. Mechanistically, NEDD4L ubiquitinates DPP4 at the K583 site to promote its degradation, and DPP4 overexpression reversed the anti-inflammatory effects of NEDD4L. Collectively, NEDD4L is consistent with acting as a negative regulator of Th2-linked inflammation, potentially via ubiquitination-mediated degradation of DPP4. - Source: PubMed
Publication date: 2026/04/09
Lv PingLi DandanSong WeiWang Jizhe