JunB (Phospho_Ser259) Antibody
- Known as:
- JunB (Phospho_Ser259) Antibody
- Catalog number:
- E011027-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- JunB (Phospho_Ser259) Antibody
Related genes to: JunB (Phospho_Ser259) 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 (Phospho_Ser259) Antibody
Related articles to: JunB (Phospho_Ser259) Antibody
- E3 ubiquitin ligases recognize substrates through specific interfaces. Accurate delineation of these interfaces is essential, as mutations disrupting them impair protein ubiquitination and drive cancer progression. However, available E3-substrate interface data are sparse and systematic prediction methods remain lacking. Here, we propose MetaESI, a deep learning framework that simultaneously predicts E3-substrate interactions and leverages its interpretable architecture to infer binding interfaces de novo. With a two-stage meta-learning strategy, MetaESI generalizes across diverse E3s and achieves state-of-the-art performance in both interaction and interface prediction. We applied MetaESI at the proteome scale to generate MetaESI-Atlas, which comprises 68,056 annotated interactions across eight species. Integrating multi-omics data, we identified mutations at MetaESI-predicted interfaces that disrupt E3-substrate binding, and experimentally validated representative examples including JunB Q244E and SPOP F102C as oncogenic drivers. By combining interpretable AI with mechanistic insight, MetaESI establishes a methodological paradigm for interpretable model design and a foundational resource for precision oncology and targeted protein degradation. - Source: PubMed
Publication date: 2026/05/20
Li DiankeZhang YutingLiu YuanZhang ZihaoQu YingjieLi JiajunJiang LinyangDiao LihongZhang ZidingZhang LingqiangCui Chun-PingLi Dong - N6-(2-hydroxyethyl) adenosine (HEA), the main active component of Cordyceps species, has garnered attention for its multifaceted hypolipidemic and antihyperglycemic activities. However, the influence by which HEA affects the progression of nonalcoholic fatty liver disease (NAFLD) remains unclear. This study sought to investigate the efficacy and mechanisms of HEA in treating NAFLD. The mouse NAFLD models were induced by high-fat diet feeding or methionine-choline-deficient diet feeding. AML12 and HepG2 cells were used for the in vitro study. Lipidemic and glycemic parameters, untargeted lipidomic, cellular thermal shift assay, and so forth were used to explore the beneficial effects of HEA in NALFD. HEA effectively alleviated the progression of NAFLD by regulating glucolipid metabolism and insulin resistance both in vitro and in vivo. Lipidomic data suggested that HEA markedly reduced triglyceride levels by blocking hepatic de novo lipogenesis and shifting fatty acids into mitochondria for oxidation and into structural lipids. Moreover, stimulation of the supernatant of adipocytes with HEA was more effective than treatment with HEA only in terms of hepatic de novo lipogenesis in HepG2 cells. Mechanistically, HEA significantly reduced the population of JunB+ adipocytes, which exerts lower thermogenic capacity. Further studies verified that HEA interacted with ASP-12, ASP-13, and TYR-15 of JunB subunits through hydrogen bonding, leading to activated PGC-1α activity and governing thermogenic adipocyte heterogeneity and consequent biological responses. These findings highlight the capacity of HEA to alleviate NAFLD through the JunB pathway, paving a new way to treat NAFLD by influencing adipocyte functionality. - Source: PubMed
Publication date: 2026/05/20
Zhang KeyanLu MengdieYang YanHuang JingpingLi LiyinYan YishuLi RuiyiYang Jing - 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