Ask about this productRelated genes to: KDM3B antibody
- Gene:
- KDM3B NIH gene
- Name:
- lysine demethylase 3B
- Previous symbol:
- C5orf7, JMJD1B
- Synonyms:
- KIAA1082, NET22
- Chromosome:
- 5q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-21
- Date modifiied:
- 2016-10-05
Related products to: KDM3B antibody
Related articles to: KDM3B antibody
- Immunotherapy has emerged as a promising therapeutic option for cancer management, but its applicability in patients with triple-negative breast cancer (TNBC) is limited by the low efficacy due to the immunosuppressive tumor microenvironment (TME). Here, we identify lysine demethylase 3B (KDM3B) as an essential mediator of immune evasion in TNBC. KDM3B expression is negatively correlated with cytotoxic T lymphocyte (CTL) infiltration. Genetic or pharmacologic inhibition of KDM3B facilitates the recruitment and activation of CD8 T cells, thereby suppressing tumor growth in TNBC mouse models. Mechanistically, KDM3B targets SHP1 by reducing H3K9me2 levels at its promoter. Suppression of KDM3B attenuates SHP1-mediated STING inactivation, which triggers robust type I interferon (IFN) responses. Strikingly, both KDM3B depletion and treatment with the KDM3B-selective inhibitor P3FI-90 significantly suppresses tumor progression and mitigates resistance to immune checkpoint blockade (ICB) therapy. Taken together, these findings establish KDM3B as a key regulator of immune escape, and targeting KDM3B represents a promising strategy to augment the efficacy of immunotherapy for TNBC. - Source: PubMed
Publication date: 2026/05/27
Wang XiaolongLi WenhaoWang YifeiZhang NingChen BingZhao WenjingWang LijuanLuo DanYang Qifeng - Minor zygotic genome activation (ZGA) is crucial for early development and totipotency acquisition; however, the regulatory mechanisms controlling minor ZGA gene expression remain elusive. Here, we show that mouse minor ZGA is driven by spatiotemporally dynamic regulation of H3K9 dimethylation (H3K9me2). H3K9me2 levels at the minor ZGA gene loci are reduced at the early two-cell stage and are reestablished by the morula stage. Maternal depletion of the H3K9 demethylases KDM3A and KDM3B leads to increased H3K9me2 levels and impaired minor ZGA at the early two-cell, followed by arrest at the two-cell to four-cell stage. In mouse embryonic stem cells, H3K9 at the minor ZGA loci is dimethylated. Combined loss of the H3K9 methyltransferases G9a and SETDB1 results in the synergistic derepression of minor ZGA genes. Mechanistically, SETDB1 targets the transcriptional factor Dux, while G9a broadly represses minor ZGA genes through H3K9me2 deposition linked to lamina-associated heterochromatin formation. Therefore, H3K9me2 dynamics are unveiled as an important regulator of minor ZGA, highlighting the indispensable role of epigenetic control in early embryogenesis. - Source: PubMed
Publication date: 2026/05/26
Maeda RyoKuroki ShunsukeShimojo HiromiNagano MasahiroMatsuwaka MasahiroSasaki HiroshiInoue AzusaTachibana Makoto - Diets-Jongmans syndrome (DIJOS) is a genetic, autosomal dominant condition caused by variation in the KDM3B gene on chromosome 5q31. Intellectual developmental disorder (IDD) is typically described as a key feature of the condition. This case series aimed to characterize the broader neuropsychological profile of DIJOS. - Source: PubMed
Donaldson SaraLong BrianWolff BrittanyMcKenzie CathrynClark MelanieMitchelson BreeMilnes Timothy SMarshall-Cary ChloeClarke DanielStrikwerda-Brown Cherie - Integration of Epstein-Barr virus (EBV) DNA into the human genome is a critical event in nasopharyngeal carcinogenesis. Here, we comprehensively characterize large-scale virus-human integration events in three EBV-positive nasopharyngeal carcinoma (NPC) cell lines and one patient NPC tumor using Nanopore long-read sequencing technology. We identified four distinct integration types, with Type A being particularly prevalent, characterized by the integration of a single fragment of the EBV genome followed by human DNA. Our findings reveal the involvement of multiple integration events in inducing inter-chromosomal translocations, leading to significant genomic disruption through chromosomal rearrangements. Additionally, we explore the relationship between EBV integration sites and structural variations, further supporting the role of EBV integration in driving genomic instability. By integrating RNA-seq data, we demonstrate the potential for EBV integration to disrupt gene expression, highlighting several integration sites within cancer-associated genes such as CD96, ARHGAP27, ASH1L, KDM3B, ZMYM2, and PIK3C2A. Notably, EBV-human fusion events were prevalent in EBV-associated NPCs, including intriguing fusion transcripts such as LRRC8C-RPMS1 and LINC00486-RPMS1, which provide further evidence of the oncogenic potential of EBV integration. Taken together, this study uncovers EBV integration patterns in Nasopharyngeal carcinogenesis using long-read sequencing technology. - Source: PubMed
Publication date: 2026/05/12
Kardan ZahraKadam AdwayChai Annie Wai YeengCheong Sok ChingLoganathan Sampath Kumar - Dysregulation of histone modifications contributes to the development of cancer. The loss of methylation on histone H3 and H4 and the loss of acetylation serve as indicators of tumors. Histone demethylase KDM3B, which contains a JmjC domain, plays an important role in tumorigenesis and development by removing H3K9me1/2 methylation. It also has a significant impact on regulating different types of cancer. KDM3B's role in prognosis and tumor formation in cancer has not been thoroughly studied. In this study, we analyzed KDM3B expression data from the TCGA database in a pan-cancer analysis. Our results show that KDM3B is highly expressed in many cancer types and is closely associated with poor prognosis. KDM3B expression is associated with immune checkpoint activities, lymphocyte infiltration, and immune landscape changes, suggesting that KDM3B could be a target for cancer therapy. - Source: PubMed
Zhu LipingPeng XiaoyanYu HaileFan XiaoluYe Zhoujie