JunB Antibody (Ab_79), pAb, Rabbit
- Known as:
- JunB Antibody (Ab_79), pAb, Rabbit
- Catalog number:
- A00255
- Product Quantity:
- 40ug
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- JunB Antibody (Ab_79) pAb Rabbit
Related genes to: JunB Antibody (Ab_79), pAb, Rabbit
- 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 (Ab_79), pAb, Rabbit
Related articles to: JunB Antibody (Ab_79), pAb, Rabbit
- Diabetic retinopathy (DR) is driven by chronic hyperglycemia and involves coordinated vascular, inflammatory, and neuroglial dysfunction. Müller glia are central to retinal homeostasis, yet their cell-state heterogeneity and inflammatory response programs in DR mice remain incompletely characterized at single-cell resolution. - Source: PubMed
Publication date: 2026/04/29
Ouyang ShuaiWang JingwenDu XiaolanZhang ShouyueHan ShijunXu XiaotongRen BeichenYu Weihong - The cerebral cortex shows species-specific variations in size and organization, which probably account for distinct behavioural abilities. These structural differences may reflect evolutionary changes in the developmental expression of shared genes. Here, to investigate this possibility, we used machine vision to identify and compare cell-type-specific gene expression patterns in the developing mouse and human neocortex, and in human cortical organoids. Using this approach, we identified genes with evolutionarily conserved or divergent transcriptional regulation, revealing species-specific cyto-temporal gene expression patterns. Among such genes, the transcription factor gene JUNB showed mutually exclusive expression in human progenitors and mouse neurons. Through cell-type-specific gain- and loss-of-function experiments in mice and human cortical organoids, we show that JUNB bidirectionally controls human cortical features, including progenitor proliferation rates, neuronal production timing and total neuronal output. We identify IRF1 as a human radial glia-specific regulator that, when expressed in mouse radial glia, activates JUNB and recruits human-like gene regulatory networks, demonstrating cross-species activation of poised developmental programmes. Together, these findings reveal how cyto-temporal regulation of shared genes drives species-specific cortical features, and provide a molecular framework for understanding and manipulating these evolutionary programmes. - Source: PubMed
Publication date: 2026/05/13
Javed AwaisGómez LucíaPravata VeronicaSarhadi MoeinGiudice Quentin LoSzalai TiméaAubert LéaRibierre ThéoNguyen LaurentCappello SilviaJabaudon DenisKlingler Esther - Yes-associated protein (YAP) condensates are critical for cell survival under hyperosmotic stress, yet how these condensates execute their specific functions remains incompletely understood. Here, we employed proximity-based proteomics to identify YAP-interacting proteins in both the diffuse and condensate-forming states. Upon YAP condensate formation, the composition of YAP-interacting proteins changed markedly. Moreover, YAP condensate components transitioned from an initial chromatin-clustering state to a subsequent transcriptional activation state. Using immunofluorescence, we verified that JUNB, TCF12, and IFI16 were enriched within endogenous YAP condensates. Notably, JUNB and TCF12 are also required for YAP condensate formation and function, as their depletion completely abolished condensate assembly and downstream gene expression. Together, these findings identify novel components essential for YAP condensate formation and illuminate their roles in the hyperosmotic stress response, providing a foundation for future therapeutic strategies targeting YAP condensates. - Source: PubMed
Publication date: 2026/05/13
Bellot Janelle SHao SiyuanLi YihuanCai Danfeng - Glucocorticoid receptor (GR) signaling elicits diverse transcriptional responses through dynamic and context-dependent interactions with chromatin. Here, we define a temporally resolved and mechanistically integrated framework for GR-mediated gene regulation. Time-resolved analyses identify three conserved classes of GR chromatin binding (sustained, transient, and late), distinguished by differences in motif strength, chromatin accessibility, and cofactors engagement. Early GR binding preferentially occurs at high-affinity glucocorticoid response elements (GREs) within pre-accessible regulatory regions, whereas late binding is associated with weaker motifs and requires chromatin remodeling activity. Enhancer activation, marked by H3K27ac deposition, closely tracks GR occupancy, supporting a model in which GR recruits acetyltransferase activity to drive coordinated enhancer activation. Concurrently, GR-centered interaction networks are dynamically reconfigured, and motif enrichment analyses identify distinct transcription factor signatures across binding classes, including AP-1/JUNB at transient sites and CEBP family members at late-binding regions. Integration of chromatin binding, chromatin interaction, and transcriptomic datasets reveals that temporal and combinatorial GR occupancy is functionally linked to gene expression programs. Distinct GR binding clusters are nonrandomly associated with specific transcriptional trajectories, including sustained, transient, and late gene induction. Moreover, combinatorial occupancy across multiple regulatory elements correlates quantitatively with transcriptional output, indicating that GR functions not as a simple binary regulator, but as an integrator of multilayered regulatory inputs. These findings support a unified model in which temporal binding dynamics, chromatin state, and combinatorial enhancer activity collectively encode transcriptional specificity, providing a general framework for stimulus-responsive nuclear receptor signaling. - Source: PubMed
Publication date: 2026/04/24
Stavreva Diana AKim SohyoungFujiwara SaoriMcGowan AndrewBaek SongjoonRinaldi LorenzoJohnson Thomas APuglia MicheleBlagoev BlagoyDequiedt FranckHager Gordon LFettweis Gregory - Background Prostate cancer (PCa) exhibits significant ancestry-related disparity. While men of African ancestry experience higher overall mortality rates, this difference is most pronounced in Sub-Saharan Africa and for grade group 1 (GG1) disease, alluding to ancestry-specific biology. Despite this health disparity, African-relevant and prostate tumour GG1 inclusive data, specifically transcriptomic data, is lacking. In turn, this raises significant concerns with regards to adopting Eurocentric models to classify and manage assumed indolent disease for African men. The risk - suboptimal treatment decisions. Methods Using a single technical and analytical pipeline, we generated total RNA sequencing data from fresh-frozen prostate tissue for 68 Black South African (40 GG1-PCa, 28 non-PCa) and 48 Australian European men (all GG1-PCa), performing ancestry-specific differential gene expression and pathway analysis. Sourcing public data enabled limited African American inclusive The Cancer Genome Atlas cross-validation (13 of 61 GG1-PCa), while Pan Prostate Cancer Group European ancestral data provided for deeper cross-ancestral comparative analyses (106 GG1-PCa, 17 non-PCa). Results Identifying 5,652 differentially expressed genes between African and European ancestral GG1 tumours ( < 0.05), including top-ranked PCa tumour suppressor genes , and downregulated in African tumours. In turn, six metabolic and six immune-related pathways showed significant African-specific negative enrichment. Concordantly, cell type analysis showed significantly lower immune, stromal, and angiogenesis scores in African over European-derived GG1 tumours. Inclusion of African American GG1 data showed pathway over gene-level ancestry-specific concordance, with significant negative enrichment verification for oxidative phosphorylation, fatty acid metabolism and glycolysis. Compared to and irrespective of PCa status, our African tissues showed a 4.9-fold increase in differential gene expression in PSA-high versus PSA-low tissues. Notably, cell type clustering revealed 29% of PSA-high non-PCa tissues exhibited cancer-like profiles, indicating potential occult disease. Conclusions Revealing substantial transcriptomic divergence from European ancestral GG1 tumours, we identify African-specific transcriptomic features that may contribute to outcome disparities in this under-appreciated clinical group. Our study highlights not only a critical shortcoming in providing equitable PCa care for African men, but it also raises major concerns with regards to managing and treating African men using European-developed criteria. - Source: PubMed
Publication date: 2026/04/24
Jensby Eva FerlevUthayopas KorawichHasan Md MehediLouw MelanieMutambirwa Shingai B AStricker PhillipCampbell RaymondLamy PhilippeMarchionni LuigiBornman M S RianaPapenfuss AnthonySørensen Karina DHayes Vanessa M