Ask about this productRelated genes to: JunB antibody
- 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
Related articles to: JunB antibody
- Senescent cells accumulate with age following stress-induced cell cycle arrest triggered by DNA damage, oncogene activation, and replicative exhaustion. While they contribute to tissue repair and tumor suppression, their persistent senescence-associated secretory phenotypes (SASPs) drive age-related diseases. The heterogeneity of senescent cell populations, particularly the distinction between primary and secondary senescence, remains incompletely understood at single-cell resolution. Here, we established models of primary senescence by X-ray irradiation of human renal epithelial cells and secondary senescence by exposing proliferating cells to conditioned media from primary senescent cells. Single-cell RNA sequencing revealed structured transcriptional trajectories culminating in distinct terminal clusters in primary (C5, C6, and C8) and secondary (C3, C5, and C7) senescence. Primary senescence preferentially converged on extracellular matrix- and fibrosis-associated programs, whereas secondary senescence exhibited more inflammatory and signaling-responsive programs, while both contexts shared a partially overlapping transcriptional module enriched in stress-response and cytokine-related transcriptional modules. We identified subtype-associated genes distinguishing primary from secondary senescent cells, as well as candidate transcriptional regulators-such as HMGA1, NFKB1, and JUNB-associated with conserved and context-specific senescence programs. This study provides a single-cell-resolved transcriptional map of divergent and shared molecular features relevant to renal aging and disease. - Source: PubMed
Jang Dong-HyunShim EunhaShin Ji-WonKim SeokhoCiotlos SerbanKim Hyun JungGil Tae-HwanKim YuminJeon Ok Hee - 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