KDM3B Antibody - N-terminal region (ARP33022_P050)
- Known as:
- KDM3B Antibody - N-terminal region (ARP33022_P050)
- Catalog number:
- arp33022_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KDM3B Antibody - N-terminal region (ARP33022_P050)
Related genes to: KDM3B Antibody - N-terminal region (ARP33022_P050)
- 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 - N-terminal region (ARP33022_P050)
Related articles to: KDM3B Antibody - N-terminal region (ARP33022_P050)
- Lung adenocarcinoma (LUAD), a leading cause of cancer mortality, involves incompletely understood epigenetic-metabolic crosstalk. We identified ANP32E as a key regulator through multi-omics (TCGA, scRNA-seq) and clinical analyses, finding its overexpression correlates with poor prognosis. Functionally, ANP32E knockdown suppressed proliferation, migration, and glycolysis in LUAD cells (A549/H1975) and attenuated xenograft growth, while overexpression promoted tumorigenesis. Mechanistically, ANP32E transcriptionally upregulates histone demethylase KDM3B, reducing repressive H3K9me2 marks at the EGFR promoter to enhance EGFR transcription. This activates PI3K/AKT signaling, inducing inhibitory GSK3β phosphorylation. Combined with ANP32E-mediated GSK3β suppression, this dual inactivation liberates oncogenic glycolysis. Crucially, KDM3B silencing or EGFR inhibition (Cetuximab) abrogated ANP32E-driven phenotypes. High-throughput screening identified Penta-O-galloyl-β-D-glucose (PGG) as an ANP32E-targeting compound, with molecular dynamics confirming binding. PGG dose-dependently inhibited the ANP32E/KDM3B/EGFR axis in vitro and suppressed tumor growth in vivo. Thus, ANP32E drives LUAD progression via KDM3B/EGFR-mediated GSK3β inactivation, representing a prognostic biomarker and therapeutic target validated by PGG. - Source: PubMed
Publication date: 2026/04/14
Wang ZhongliangLi QianxiaYe ZeguangWu XiFang CanJiang WenyangZhu Min - A 5-year-3-month-old boy presented with intellectual disability, autism spectrum disorder, short stature, long ears, large auricles, a broad nasal tip, a pointed chin, and cryptorchidism. Whole-exome sequencing revealed a likely pathogenic heterozygous missense variant in (c.5147T>C, p.Leu1716Pro), supporting a diagnosis of Diets‑Jongmans syndrome. This case further enriches the mutation spectrum of Diets‑Jongmans syndrome and suggests that early genetic testing helps clarify the etiology in children with developmental delay or intellectual disability, autism spectrum disorder, and short stature. - Source: PubMed
Shen Ke-XinXiang Yan-JieWang JinRen Kang-YiDing Yuan - Pathogenic variants in have been implicated as the cause of Diets-Jongmans syndrome (DIJOS), an autosomal-dominant disorder characterized by growth retardation, intellectual disability, facial dysmorphism and autism-spectrum disorder. However, only a limited number of cases have been reported. - Source: PubMed
Publication date: 2026/02/28
Miao HaixiaZhang TingChen ShuaiXu XiaochaFang KexinWu DingwenZhang YiHuang Xinwen - Diets-Jongmans syndrome (DIJOS) is a rare neurodevelopmental disorder associated with heterozygous variants in . The phenotypic spectrum continues to expand as additional individuals are identified. - Source: PubMed
Publication date: 2026/02/06
Deligozoglu DuyguGenc AslýKýlýc EsraTepe DeryaKocaay Pýnar - Endocrine-resistant estrogen receptor-positive (ER) breast cancer often presents with an immune-cold phenotype, yet the upstream regulators driving immune evasion remain unclear. GNAL, a G-protein subunit involved in calcium signaling, has emerged as a potential player in modulating the tumor immune microenvironment, but its role in ER breast cancer has not been systematically investigated. This study aims to systematically investigate GNAL's biological functions, molecular mechanisms, and prognostic relevance in endocrine-resistant ER breast cancer, as well as its role in regulating the tumor immune microenvironment. - Source: PubMed
Publication date: 2026/01/26
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