JMJD1B KDM3B antibody Ab host: Rabbit
- Known as:
- JMJD1B KDM3B (anti-) Antibody production species: Rabbit
- Catalog number:
- 'AP23894PU-N
- Product Quantity:
- 50 Вµg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- JMJD1B KDM3B antibody host: Rabbit
Related genes to: JMJD1B KDM3B antibody Ab host: Rabbit
- 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
- Gene:
- PPP1R18 NIH gene
- Name:
- protein phosphatase 1 regulatory subunit 18
- Previous symbol:
- KIAA1949
- Synonyms:
- phostensin
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-02
- Date modifiied:
- 2016-10-05
Related products to: JMJD1B KDM3B antibody Ab host: Rabbit
Related articles to: JMJD1B KDM3B antibody Ab host: Rabbit
- The periodontal ligament (PDL) is a mechanosensitive connective tissue that provides tooth support and oral function. Although mechanical stress regulates PDL cell behavior, the transcriptional response of PDL cells to hydrostatic pressure (HP) remains poorly understood. This study aimed to characterize the transcriptomic changes induced by HP in human PDL cells and to identify the mechanotransduction pathways associated with epigenetic regulation. - Source: PubMed
Publication date: 2026/07/09
Miyano TakashiKaku MasaruSera Toshihiro - Non-functioning pituitary adenomas (NFPAs) present a complex clinical challenge due to their indolent and invasive growth patterns, and critical anatomical location. Post-surgical tumor progression is frequent in patients with NFPAs, which often necessitates additional therapeutic interventions. The molecular mechanisms underlying post-surgical progression remain poorly understood and there are currently no reliable methods to stratify patients according to risk of tumor progression. The aim of this study was to comprehensively characterize the molecular alterations, together with an integrated understanding of their interactions, that could potentially uncover the biological processes driving post-surgical tumor progression of NFPAs. - Source: PubMed
Publication date: 2026/06/23
Suman MedhaHallén TobiasGarner TerenceThorsell AnnikaStevens AdamKöster LinusCarén HelenaRagnarsson OskarSkoglund ThomasJohannsson Gudmundur - 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
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