JMJD5 antibody - N-terminal region (ARP33597_P050)
- Known as:
- JMJD5 (anti-) - N-terminal region (ARP33597_P050)
- Catalog number:
- arp33597_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- JMJD5 antibody - N-terminal region (ARP33597_P050)
Related genes to: JMJD5 antibody - N-terminal region (ARP33597_P050)
- Gene:
- KDM8 NIH gene
- Name:
- lysine demethylase 8
- Previous symbol:
- JMJD5
- Synonyms:
- FLJ13798
- Chromosome:
- 16p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-17
- Date modifiied:
- 2019-03-19
Related products to: JMJD5 antibody - N-terminal region (ARP33597_P050)
Related articles to: JMJD5 antibody - N-terminal region (ARP33597_P050)
- Soybean (Glycine max) is a photoperiod-sensitive legume whose latitudinal adaptation depends on the precise control of flowering time and plant height. Histone demethylases of the JmjC domain-containing (JMJ) protein family have been implicated in these processes across plant species, but their specific roles in soybean remain largely unexplored. Here, we identify soybean GmJMJ19 and GmJMJ20, two closely related JMJD5/KDM8 orthologs, as master epigenetic regulators that coordinately control both photoperiodic flowering and post-flowering plant height. Both genes exhibit intrinsic, rhythmic expression peaking at ZT12, and their encoded proteins physically interact with the florigen proteins FT2a and FT5a. Loss-of-function mutants display delayed flowering under long days (LDs) and increased plant height under both LDs and short days (SDs), whereas overexpression phenocopies the mutant flowering phenotype, indicating revealing a critical dosage requirement for proper function. Mechanistically, GmJMJ19 and GmJMJ20 are recruited by the FT/FD transcriptional complex to directly activate AP1a and AP1c expression through chromatin modulation. Population genomic analyses reveal distinct selection signatures: GmJMJ19 underwent sustained directional selection during cultivation, whereas GmJMJ20 experienced an early domestication sweep with limited subsequent change. Haplotype analysis identifies coordinated latitudinal clines, with the JMJ19/JMJ20 combination predominating at high latitudes to promote early flowering and limit height, while JMJ19/JMJ20 and wild JMJ19/JMJ20 alleles prevail at low latitudes, conferring later flowering and increased height. Collectively, our findings establish GmJMJ19 and GmJMJ20 as central chromatin regulators linking florigen signaling to downstream target expression and provide valuable allelic resources for breeding regionally adapted soybean varieties across a wide range of latitudinal environments. - Source: PubMed
Publication date: 2026/09/09
Liu XiulinSong ChengyangCui YuanyuanSun YuMa XiaofeiLuo QianyiRong XuanZhang ZhaohanDeng Xing WangLuo Xiao - In solid tumors, hypoxia is a key driver of metastasis by promoting cellular plasticity and chromosomal instability (CIN). Despite this, the mechanisms by which malignant cells concurrently co-opt these elements of hypoxic adaptation to promote metastasis remains unclear. Here we report that hypoxia promotes metastasis by suppressing the JmjC-containing histone lysine demethylase KDM8. Kdm8 targeting in a Kras;Trp53-driven mouse model of pancreatic ductal adenocarcinoma induces a profound loss of the epithelial morphology and widespread metastatic disease. Mechanistically, Kdm8 suppression in normoxia recapitulates major aspects of the global epigenetic changes, transcriptomic rewiring, and mitotic spindle defects induced by hypoxia. Of note, disruption of Kdm8's demethylase function phenocopies the effects of Kdm8 loss, whereas expression of hypermorphic Kdm8 variants that are resistant to hypoxic suppression reduces metastasis beyond the levels achieved by the wildtype counterpart. Through the suppression of Kdm8 demethylase activity, hypoxia unleashes a potent metastatic program by simultaneously advancing cellular plasticity and CIN. - Source: PubMed
Publication date: 2026/07/30
Gunasekaran Pradeep MoonWang QianqianGuseva PolinaChang Yoke-ChenChauhan RajikaKley AlexanderXu MengdieLee GeneMarshall GregoryGhosh Roy SiddharthMasoudpoor YousefLi OscarRoberts ArthurWalton Kelly WatkinsFranciosa LucyannBhat ShafiqZachariah EmmanuelPatel KishanZhou ZhongrenCao JianChen WenjinNi Julie ZhouliGu Sam GuopingMontagna CristinaChiou Shin-Heng - Platinum-based chemotherapy remains a cornerstone in the treatment of advanced non-small cell lung cancer (NSCLC), yet its efficacy is frequently limited by drug resistance. JMJD5 (Jumonji Domain-Containing Protein 5) is a multifunctional protein implicated in tumor progression with enzymatic and non-enzymatic activities. While it has been reported to enhance the sensitivity of NSCLC cells to EGFR tyrosine kinase inhibitors (TKIs), its function in modulating response to conventional platinum chemotherapy is unknown. - Source: PubMed
Publication date: 2026/07/17
He JingWei HaohaoLi TaoXiao QiuxiangLiu Guiling - Despite advances in multimodal treatment, head and neck squamous cell carcinoma (HNSCC) remains a major clinical problem owing to its high recurrence rate and frequent development of treatment resistance. Abnormal histone modifications, particularly lysine methylation regulated by methyltransferases (KMTs) and demethylases (KDMs), have emerged as key drivers of HNSCC initiation, progression, and cellular plasticity. This review aims to comprehensively evaluate the role of selected KMTs and KDMs in HNSCC biology, with a focus on their contribution to resistance to immunotherapy, radiotherapy, and cytotoxic chemotherapy. We summarize and critically analyze preclinical and clinical studies investigating histone methylation dynamics in HNSCC, with particular emphasis on enzymes such as KMT2C/D, EZH2, NSD1/NSD2, SMYD3, G9a/EHMT2, LSD1, KDM2A/B, KDM3, KDM4, KDM5, KDM6, KDM7, and KDM8. Attention is given particularly to pharmacological approaches targeting these proteins: we discuss small-molecule inhibitors of EZH2, LSD1, KDM4/5/6, and other KMT/KDMs that are currently in preclinical development or in early clinical trials, and we highlight completed and ongoing studies testing EZH1/2 inhibitors and epigenetic combinations in patients with recurrent and metastatic HNSCC. The deregulation of specific KMTs and KDMs reshapes histone methylation at key residues, thereby controlling cell cycle progression, epithelial-mesenchymal transition (EMT), stem cell phenotypes, DNA damage responses, and multiple interactions with the immune system in HNSCC. Targeting disrupted histone methylation pathways may partially reverse the epigenetic reprogramming of HNSCC cells and represents a promising strategy to improve treatment efficacy in patients with advanced disease. We also summarize the preclinical evidence and the currently limited clinical data on targeting histone methylation dynamics in HNSCC and discuss their therapeutic implications. - Source: PubMed
Publication date: 2026/07/06
Adamczuk KamilaMiziak PaulinaAdamczuk GrzegorzBaran MarzenaNees MatthiasStepulak Andrzej - iPSCs have drawn significant attention for their biomedical potential, yet reprogramming remains inefficient and the underlying mechanisms are incompletely defined. KDM8, a histone demethylase, is known to play critical roles in processes such as cell-cycle regulation and embryonic development; nevertheless, its function in reprogramming has not been reported. Our investigations demonstrate that KDM8 significantly enhances the reprogramming efficiency mediated by the canonical Yamanaka factors. Remarkably, KDM8, in combination with OCT4 alone, is sufficient to reprogram somatic cells. Further analyses reveal that KDM8 facilitates reprogramming through a dual regulatory mechanism. On one hand, KDM8 leverages its canonical enzymatic activity to reduce the epigenetic barriers to iPSC formation. More importantly, KDM8 functions as a co-regulator of the transcription factor SOX2, promoting SOX2's DNA-binding affinity and transcriptional regulation of downstream pluripotency target genes. Accordingly, we propose a novel regulatory framework that uncovers novel mechanisms and functions of KDM8 in cellular reprogramming. - Source: PubMed
Publication date: 2026/06/18
Yang SongqinYe ZhikaiLin LuJiang ZhenlongWang ErkangWang Jin