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)
- 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 - Both KDM8 and c-Myc have been implicated in regulating tumor glucose metabolism. However, whether there is an interaction between KDM8 and c-Myc, and whether KDM8 function is dependent on c-Myc in ovarian cancer (OC) remains unclear. Paired cancerous and paracancerous tissues from five OC patients were analyzed for KDM8 and c-Myc expression using reverse transcription quantitative polymerase chain reaction and Western blot. Co-Immunoprecipitation assays were conducted to verify their potential interaction. Stable OVCAR3 and SKOV3 cell lines overexpressing KDM8 or c-Myc were established. Functional assays (CCK-8, Transwell, colony formation, wound healing, and flow cytometry) were performed to assess proliferation, migration, invasion, colony formation, and apoptosis. Metabolic changes were evaluated by measuring glucose uptake and lactate accumulation using colorimetric and ELISA kits, respectively. Finally, a nude mouse subcutaneous xenograft model was constructed to observe the growth and metabolic levels of OC in vivo. Both mRNA and protein levels of KDM8 and c-Myc were significantly upregulated in ovarian cancer (OC) tissues compared to paracancerous tissues. Furthermore, a direct interaction between KDM8 and c-Myc was identified. Functionally, KDM8 and c-Myc synergistically promoted the malignant behavior of OC cells, including enhanced proliferation, migration, invasion, and colony formation capacities. Additionally, they promoted metabolic reprogramming, as evidenced by increased glucose uptake and lactate accumulation, while concurrently inhibiting apoptosis. However, siRNA-mediated knockdown of c-Myc significantly attenuated these oncogenic effects, reversing the enhanced proliferative, migratory, and metabolic capacities of OC cells. In vivo experiments further verified that the KDM8 /c-Myc axis affects OC growth and metabolic levels. Collectively, our findings indicate that KDM8 and c-Myc cooperate to promote OC progression, which may be mediated through the regulation of glucose metabolism. Notably, KDM8 function is partially dependent on c-Myc in this context. These results provide preliminary evidence supporting KDM8 as a potential candidate target for OC diagnosis and treatment, with further validation required in larger cohorts. - Source: PubMed
Publication date: 2026/04/27
Liu ChunyanXu QianLi ZhuolingYang XiaoliMao BiboGuo LiliLiu XinLiu Wenyuan