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)
- KDM8 is a histone demethylase initially characterized for its activity on H3K36me2, although its function is now more widely recognized as a hydroxylase. Through a high-throughput screening on histone demethylases, we identified KDM8 as a regulator of the γH2AX response following ionizing radiation. Experiments using specific reporter substrates revealed that KDM8 depletion increases homologous recombination (HR), while its overexpression reduces HR. This shift is counterbalanced by a concomitant decrease in non-homologous end joining (NHEJ), an effect partly independent of its demethylase activity and unrelated to cell cycle alterations. Despite this imbalance, cellular sensitivity to DNA-damaging agents - such as ionizing radiation, mitomycin C, and camptothecin - remains unchanged. FRET experiments in living cells demonstrated an interaction between KDM8 and Rad51 after DNA damage induced by camptothecin. These findings identify KDM8 as a key player in DSB repair, specifically influencing HR. - Source: PubMed
Publication date: 2026/04/19
Fages JérémieBergoglio ValérieJulia EmmanuelCintori LuanaChailleux CatherineFourez Anne-LisePonsolle NatachaTrouche DidierCanitrot Yvan - Hypertrophic cardiomyopathy (HCM) is a prevalent cardiovascular disorder affecting populations worldwide, characterized by abnormal thickening of the heart muscle.(Supporting S1) The development of HCM is influenced by multiple factors, including genetic mutations, geographical conditions, lifestyle, and environmental exposures. The availability of extensive genomic datasets in public repositories provides an opportunity to identify potential genetic contributors and functional biomarkers associated with HCM. Previous studies have highlighted the pivotal role of the MYBPC3 gene in the pathogenesis of HCM. In this study, computational analyses were performed to predict gene mutations and functional biomarkers using RNA-sequencing and whole exome sequencing datasets. A total of 12 RNA-sequencing samples, comprising four healthy controls and eight HCM cases, along with 12 exome sequencing datasets, were retrieved from the Gene Expression Omnibus (GEO) database. RNA-sequencing analysis identified the top 20 differentially expressed genes associated with HCM, including MIB2, ZBTB48, MYBPC3, PRPF40B, CD27-AS1, MYH7, WDR90, KDM8, BCAM, ZSWIM9, KANK3, CCDC85A, ZNF512B, POLR3H, NUP210, PSMG4, GPLD1, GNL1, SH2D3C, and COL4A6. Among these, MYH7 exhibited the highest expression level, showing strong similarity to MYBPC3 in its association with HCM. Whole exome sequencing analysis further identified a panel of variant genes including MYBPC3, MYH6, MYH7, TNT, Titin, Desmin, ACE1, TGF-beta, Ang-2, SGCG, SGCA, DMD, and LaminA/C, all previously implicated in HCM pathophysiology. This integrative study underscores the correlation between differential gene expression patterns and clinical variants in HCM, providing valuable insights into the molecular mechanisms underlying the disease. - Source: PubMed
Publication date: 2025/11/21
Cn PrashanthaR RamachandraNm GuruprasadReddy Vaddi Damodara - In most solid tumors, hypoxia is a critical physical attribute that reprograms malignant cells into a highly metastatic state. Specifically, hypoxia is a well-established inducer of cellular plasticity, which is associated with treatment resistance and metastasis. Furthermore, hypoxia exacerbates chromosomal instability (CIN), a hallmark of cancer that can be initiated by the loss of and a key contributor to metastasis. Despite this, the mechanisms by which malignant cells concurrently co-opt these elements of hypoxic adaptation to promote metastasis remains unknown. Here we report that hypoxia promotes metastasis by suppressing the JmjC-containing histone lysine demethylase Kdm8. CRISPR/Cas9-mediated targeting of in a ;-driven mouse model of pancreatic ductal adenocarcinoma robustly rewires the malignant cell transcriptomic programs, leading to a profound loss of the epithelial morphology and widespread metastatic disease. Mechanistically, suppression in normoxia recapitulates major aspects of the global epigenetic changes and the transcriptomic rewiring induced by hypoxia. Moreover, deficiency leads to mitotic defects, increased micronuclei formation, copy number gains, and enhanced CIN. Of note, disruption of Kdm8's demethylase function phenocopies the effects of 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: 2025/10/01
Gunasekaran Pradeep MoonWang QianqianChang Yoke-ChenGuseva PolinaChauhan RajikaKley AlexanderLee GeneRoy Siddharth GhoshMasoudpoor YousefRoberts ArthurWalton Kelly WatkinsFranciosa LucyannBhat ShafiqZachariah EmmanuelPatel KishanZhou ZhongrenChen WenjinNi Julie ZhouliGu Sam GuopingMontagna CristinaChiou Shin-Heng - In most solid tumors, hypoxia constitutes a defining microenvironmental feature that reprograms malignant cells into a highly metastatic state by driving cellular plasticity and exacerbating chromosomal instability (CIN). However, the mechanisms by which cancer cells concurrently co-opt these elements of hypoxic adaptation to promote metastasis remains poorly understood. Here, we report that hypoxia promotes metastasis by suppressing the JmjC-containing histone lysine demethylase Kdm8. CRISPR/Cas9-mediated targeting of in a ;-driven mouse model of pancreatic ductal adenocarcinoma (PDA) robustly rewires the malignant cell transcriptomic programs, leading to a profound loss of the epithelial morphology and widespread metastatic disease. In PDA patients, a high KDM8-induced gene signature is associated with reduced metastatic burden and better survival in advanced disease. Notably, suppression in normoxia recapitulates key aspects of the global epigenetic and transcriptomic rewiring, mitotic spindle defects, and CIN induced by hypoxia. Moreover, disruption of Kdm8's demethylase activity phenocopies loss, whereas expression of hypermorphic Kdm8 variants resistant to hypoxic suppression markedly reduces metastasis beyond the levels achieved by the wildtype protein. Through the suppression of Kdm8 demethylase function, hypoxia unleashes a potent metastatic program by simultaneously advancing cellular plasticity and CIN. - Source: PubMed
Publication date: 2025/08/29
Gunasekaran Pradeep MoonWang QianqianChang Yoke-ChenGuseva PolinaChauhan RajikaKley AlexanderLee GeneRoy Siddharth GhoshMasoudpoor YousefRoberts ArthurWalton Kelly WatkinsFranciosa LucyannBhat ShafiqZachariah EmmanuelPatel KishanZhou ZhongrenChen WenjinNi Julie ZhouliGu Sam GuopingMontagna CristinaChiou Shin-Heng - Under the combined effects of long-term natural selection and artificial domestication, Tibetan sheep on the Qinghai-Tibet Plateau have evolved distinct ecotypes to survive extreme high-altitude conditions, including hypoxia, cold, and low oxygen levels. These ecotypic variations not only serve as an ideal model for studying plateau livestock adaptation but also harbor valuable genetic diversity. However, the lack of comprehensive genetic analyses on their adaptive and phenotypic traits has hindered the effective conservation and utilization of these resources. Using whole-genome resequencing, we systematically studied seven Tibetan sheep breeds, uncovering their genetic structure and diversity. Population analyses, including NJ and maximum likelihood trees, revealed clear genetic differentiation and migration patterns. Selective sweep analyses (Fst and θπ) identified hypoxia-related genes (DOCK8, IGF1R, JAK1, SLC47, TMTC2, and VPS13A) and wool color genes (TCF25, MITF, and MC1R). GWAS further detected candidate genes for body size traits (height, length, weight), enriched in cGMP-PKG, cAMP, and Hedgehog signaling pathways. Integrating GWAS and transcriptomics, we pinpointed key wool trait genes, including WNT16 (non-synonymous mutations), PRKCA, MAP3K8, MMP7, OVOL2 (intergenic SNPs), and COL7A1, KDM8, ZNF385D (intronic SNPs). Notably, HOX family transcription factors were found to critically regulate hair follicle development. These genetic markers offer promising targets for molecular breeding to enhance wool quality and adaptive traits. Our findings provide a genetic basis for understanding Tibetan sheep's unique adaptations and production traits, supporting future breeding strategies and sustainable utilization of their genetic resources. - Source: PubMed
Publication date: 2025/07/02
Tian DehongHan BuyingLi XuePei QuanbangZhou BaichengZhao Kai