Ask about this productRelated genes to: DHRS2 antibody
- Gene:
- DHRS2 NIH gene
- Name:
- dehydrogenase/reductase 2
- Previous symbol:
- -
- Synonyms:
- HEP27, SDR25C1
- Chromosome:
- 14q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-04-26
- Date modifiied:
- 2016-05-27
Related products to: DHRS2 antibody
Related articles to: DHRS2 antibody
- Gestational diabetes mellitus (GDM) is a pregnancy-related disorder characterized by inflammatory dysregulation that disrupts maternal-fetal immune homeostasis, yet the contribution of mitochondrial dysfunction to this pro-inflammatory state remains incompletely understood. - Source: PubMed
Publication date: 2026/02/26
Zhao RuiChai TingtingGao QinJiang Aimin - This study aimed to evaluate tissue-associated circulating cell-free DNA (cfDNA) as indicators of radiotherapy-related effects and treatment-associated toxicity in prostate cancer. In addition, inter-individual variability in these markers and their responses to radiotherapy-induced cystitis and rectitis were investigated. The DNA methylation status of six tissue-associated genes representing the prostate (,), colon (,), and bladder (,) was analyzed in serum-derived cfDNA using methylation-sensitive melting curve analysis (MS-MCA). Five of the six analyzed genes demonstrated significantly higher relative DNA levels in patients with prostate cancer compared with controls. Radiotherapy did not significantly alter the relative DNA levels of these tissue-associated genes. However, cfDNA fragmentation was significantly increased in the post-treatment group compared to the pre-treatment group. Notably, 79-bp DNA fragments were significantly more abundant than 230-bp fragments. In the post-treatment group, no significant correlations were observed between cfDNA fragmentation and the relative DNA levels of most targets, except for an association between the 230-bp fragment and relative DNA levels. These findings suggest limited coupling between cfDNA fragmentation patterns and tissue-associated cfDNA release. Marked inter-individual variability in cfDNA methylation signatures was observed across all examined CpG-containing regions except . This variability did not change significantly following radiotherapy and may therefore limit the utility of these assay regions for monitoring individual radiation-induced tissue damage. Furthermore, no significant changes in methylation profiles of colon- or bladder-associated genes were detected in patients who developed radiotherapy-induced rectitis or cystitis. Overall, increased cfDNA fragmentation following radiotherapy and substantial inter-individual variability in methylation profiles across tissue-associated regions may mask tissue-associated cfDNA signals, thereby complicating the assessment of radiation-induced tissue damage. - Source: PubMed
Publication date: 2026/03/06
Bahtiyar NurtenMermut OzlemFirtina SinemOzaydin AhmetSuleymanova AishaIsikgil BegumOnaran İlhan - Clear cell renal cell carcinoma (ccRCC) is the most prevalent subtype of kidney cancer, representing about 70–80% of all renal cell carcinomas. Cuproptosis, a recently identified mode of cell death, has increasingly been linked to tumor initiation, progression, and drug resistance. Our study provides the first evidence that the histone acetyltransferase KAT2A regulates cuproptosis in ccRCC by modulating histone H3 lysine 27 (H3K27) acetylation. - Source: PubMed
Publication date: 2026/01/20
Cao YilongXu ChaoZhang BoweiQu ChangbaoLiu YuepengShi BeiLi XiaolingLi JiehanZhang ZeyuanDai ShengtaoSun QingyunWang YaxuanGu Junfei - Autism spectrum disorder (ASD) is a highly heritable neurodevelopmental disorder, yet the molecular mechanisms linking ASD-associated genes to cellular dysfunction remain incompletely understood. Among methyl-CpG binding domain (MBD) proteins, MBD5 and MBD6 are recurrently disrupted in individuals with ASD, but their roles in neuronal cells remain poorly defined. Here, we investigated the cellular and transcriptional consequences of MBD5 and MBD6 haploinsufficiency using human neuroblastoma SH-SY5Y cells. We established MBD5-and MBD6-heterozygous SH-SY5Y cell lines by genome editing and performed genome-wide transcriptome analysis. Microarray profiling revealed widespread transcriptional dysregulation characterized by predominant gene upregulation, consistent with repressive roles for both proteins. Notably, a shared subset of downregulated genes was enriched for mitochondrial-related functions, including COX17, COX4I2, DHRS2, MCUB, and PDK1. These expression changes were validated by quantitative real-time PCR. Analysis of publicly available ChIP-seq datasets further demonstrated co-localization of MBD5, MBD6, and components of the BAP1 complex at the COX17 promoter, suggesting direct chromatin-mediated regulation. Functionally, MBD5 and MBD6 haploinsufficiency impaired mitochondrial respiration, as evidenced by reduced basal and ATP-linked oxygen consumption rates without changes in mitochondrial content. Consistent with this defect, heterozygous cells exhibited severe growth impairment under galactose conditions and a compensatory shift toward glycolytic metabolism. Together, these findings uncover a previously unrecognized chromatin-mitochondria regulatory axis linking MBD5 and MBD6 haploinsufficiency to mitochondrial dysfunction, providing mechanistic insight into how epigenetic dysregulation may contribute to ASD pathogenesis. - Source: PubMed
Publication date: 2026/01/14
Meguro-Horike MakikoIwata KeikoMatsuzaki HideoHorike Shin-Ichi - Epigenetic dysregulation is a significant factor contributing to cisplatin resistance in bladder cancer (BCa). Increasing studies indicated a synergistic effect of cisplatin and Entinostat, which is an FDA-approved histone deacetylases (HDAC) inhibitor, however, the underlying mechanisms of this effect remains unknown. Herein, the synergy of cisplatin and Entinostat was confirmed in BCa cells. Integrated RNA-seq and ATAC-seq analysis revealed that the combined regimen of cisplatin and Entinostat led to significant downregulation of platinum resistance and DNA damage repair-related pathways. We focused on the candidate gene dehydrogenase/reductase member 2 (DHRS2), and found that Entinostat counteracted cisplatin resistance via promoting histone H3K18 lactylation (H3K18la)-mediated DHRS2 upregulation and enhancing the nuclear translocation of DHRS2. DHRS2 downregulation promoted cisplatin resistance by upregulating aldo-keto reductase family 1 member C3 (AKR1C3), a key enzyme in androgen synthesis. Moreover, we validated a negative correlation between DHRS2 levels and AKR1C3 expression in clinical BCa samples. It was found that high DHRS2 and low AKR1C3 expression correlates with improved neoadjuvant chemotherapy (NAC) response. Furthermore, high DHRS2 predicts better survival specifically in male patients, indicating sex-specific androgen involvement. Overall, these findings elucidate the epigenetic mechanism underlying the cisplatin-sensitizing effect of Entinostat, and identifies the DHRS2-AKR1C3-androgen axis as a potential target, particularly for male patients. - Source: PubMed
Publication date: 2025/12/09
Xu GuanghuiZheng MinghaoWu ZhigangXie TianleiLi YuqinHu GanlinFang ShutingZhang JingDiao WenliZhao WeiGuo HongqianZhuang Junlong