Ask about this productRelated genes to: JMJD3 antibody
- Gene:
- KDM6B NIH gene
- Name:
- lysine demethylase 6B
- Previous symbol:
- JMJD3
- Synonyms:
- KIAA0346
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-27
- Date modifiied:
- 2018-11-16
Related products to: JMJD3 antibody
Related articles to: JMJD3 antibody
- The efficacy of the host antiviral response against Influenza A virus (IAV), a leading cause of global pandemics, hinges upon the rapid recognition of the pathogen and the prompt activation of immune mechanisms. Nevertheless, the epigenetic landscape that orchestrates this antiviral response remains largely elusive. Here, we identify histone demethylase JMJD2D as a critical regulator in defense against IAV infection. A significant upregulation of JMJD2D expression was observed clinically in response to IAV infection, indicating that JMJD2D may play a role in regulating IAV infection. Indeed, JMJD2D-deficient mice exhibit increased susceptibility to IAV, characterized by elevated viral loads, severe lung tissue damage, and reduced survival rates, suggesting that JMJD2D plays an essential role in defense against IAV infection. Consistently, knockdown or pharmacological inhibition of JMJD2D in lung cells suppressed IAV replication and the IAV-triggered innate immune response. Mechanistically, JMJD2D suppressed IAV infection by removing H3K9me3 at the promoter region of retinoic acid inducible gene-I (RIG-I) and cooperating with NF-κB to enhance the expression of RIG-I, a critical sensor for IAV RNA. This study identifies JMJD2D as an epigenetic rheostat that governs RIG-I-mediated antiviral signaling, highlighting its potential as a therapeutic target for mitigating severe IAV infection. - Source: PubMed
Publication date: 2026/04/18
Xia XiaochunLiang JiadiGuo HanshiZhang FudongZhang JunjieYu ChundongMo PingliHong Yilin - Orthodontics is not limited to the movement of teeth, but has also expanded to the cellular and molecular realms. In this study, it was aimed to review mechanisms and implications of biological interplay between orthodontic forces and apical papilla-derived stem cells. - Source: PubMed
Publication date: 2025/11/08
Sobhani MaryamBathaei YasamanAfzalan AlirezaHormozi SepidehShanehsaz ZeinabNabizadeh SaraGashtasb Kosar - Regulatory T (Treg) cells expressing Forkhead Box P3 (FOXP3) play crucial roles in maintaining immune tolerance and tissue integrity. EZH2, a Histone H3 lysine 27 (H3K27) methyltransferase, is known as a key regulator of Treg cell identity and suppressive function upon activation. Here, we demonstrate that the H3K27 lysine demethylase KDM6B, which catalyzes the opposing reaction to EZH2, was also required for Treg cell identity and function after activation. Treg-specific deletion of Kdm6b impaired tissue Treg cell fate and function. KDM6B was upregulated following T cell antigen receptor (TCR) signaling in Treg cells and contributed to the regulation of Treg-associated gene expression through both direct and indirect mechanisms. A subset of Treg functional genes were direct targets of KDM6B and were co-occupied by FOXP3 at cis-regulatory regions, where KDM6B recruitment limited H3K27me3 accumulation. More broadly, KDM6B-dependent H3K27 demethylation facilitated Treg gene expression programs that supported tissue Treg homeostasis. - Source: PubMed
Publication date: 2026/04/23
He MinghongXu BeisiBose Pria GMcCullough Morgan JSellers Rani SZong XinyingQi WenjieBanten Brianna LTune Miriya KZimmerman Matthew PMullins Genevieve NMiller Brian CMilner J JustinWhitmire Jason KTsagaratou AgelikiShpargel Karl BDoerschuk Claire MWang Yong-DongSteele Jacob APruett-Miller Shondra MFeng YongqiangMock Jason R - The effectiveness of treatment of head and neck squamous cell carcinomas (HNSCC) is still unsatisfactory, and novel therapeutics could improve outcomes. Histone deacetylases (HDAC) and histone lysine demethylases (KDMs) emerged as important molecular targets in HNSCC. Moreover, joint inhibition of epigenetic targets may be therapeutically advantageous. Thus, the aim of this project was to evaluate the effects of combinations of panobinostat, a pan-HDAC inhibitor, with KDM4-6 inhibitors (KDMi), ML324, GSK-J4, and JIB-04. Experiments were performed in FaDu and SCC-152 cell lines. Resazurin and clonogenic assays were used to evaluate the cell viability and clonogenic potential, respectively. Apoptosis was assessed by flow cytometry after Annexin V staining. Flow-cytometric detection of γH2A.X was applied for DNA damage evaluation. Gene expression was quantified by qPCR. KDM proteins occupancy at gene promoters was measured by quantitative chromatin immunoprecipitation. KDMi enhanced the anticancer effects of panobinostat in HNSCC cell lines. The combinations of panobinostat with ML324 and JIB-04 synergistically reduced cell viability in FaDu and SCC-152 cells, and increased apoptosis induction in SCC-152 cells. These effects could be attributed to the modulation of BIRC5 and CDKN2A expression, and enhanced accumulation of DNA double-strand breaks following combinatorial treatments in FaDu cells. Decreased expression of stemness-related genes upon KDMi treatment in FaDu cells was associated with decreased binding of KDM4A and/or KDM6B at SOX2 and POU5F1 gene promoters. The suppression of stemness-associated phenotype, and the concurrent promotion of apoptosis by the studied combinations of chemicals, suggest their potential as a novel therapeutic strategy in HNSCC. - Source: PubMed
Publication date: 2026/04/20
Dorna DawidKleszcz RobertDrabarz KarolinaKubiak MałgorzataStefanska BarbaraPaluszczak Jarosław - Myopia is a global epidemic and a leading cause of visual impairment. It is driven by intermittent environmental exposures, such as near-work, which induce scleral hypoxia. However, the molecular mechanism that translates these transient stimuli into sustained myopia progression remains elusive. We hypothesized that intermittent myopiagenic exposures establish stable pathological changes in the sclera that contribute to myopia development. - Source: PubMed
Publication date: 2026/04/20
Lei YiLin XiaoleiLing XuemeiTan YuhanYuan JianLi YatingDi MengqiPan YuluZhong LurongFeng ZhaoningJiao FangfangHu ChangxiDeng HanyuPan MiaozhenSu JianzhongQu JiaChen WeiZhao FeiZhou Xiangtian