Ask about this productRelated genes to: DDX25 antibody
- Gene:
- DDX25 NIH gene
- Name:
- DEAD-box helicase 25
- Previous symbol:
- -
- Synonyms:
- GRTH
- Chromosome:
- 11q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-05-30
- Date modifiied:
- 2016-10-05
Related products to: DDX25 antibody
Related articles to: DDX25 antibody
- Cyclin-dependent kinase 9 (CDK9) is a crucial regulator of transcriptional progression of RNA polymerase-II (RNAP2). RNA polymerases trapped in DNA can be a source of transcription-replication conflict (T-R conflict), which is a common source of replication stress. AZD4573, a highly selective CDK9 inhibitor, has been shown to induce apoptosis in leukemia cell lines, while its anti-tumor potential in breast cancer has yet to be elucidated. - Source: PubMed
Publication date: 2025/07/25
Lee MinyoungLee Kyung-HunMin AhrumKim So HyeonHam SujinHwang Hae MinNoh YoulimKim Yu-JinLee Dae-WonKoh JiwonIm Seock-Ah - Gonadotropin-releasing hormone (GnRH) plays a critical role in reproductive function, with its activity influenced by differential splicing that generates functionally distinct isoforms. However, the molecular mechanisms regulating GnRH pre-mRNA processing remain poorly understood. In this study, we investigated the effects of putrescine, a biogenic polyamine, on GnRH splicing and the expression of splicing regulatory factors. Transcriptome analysis revealed that putrescine treatment induces significant changes in the expression of splicing-related genes. Notably, putrescine enhanced the expression of both the full-length GnRH isoform (GnRH V1) and an exon-skipped variant (GnRH V2), with the latter exhibiting higher expression levels. Further analysis showed putrescine significantly upregulated key alternative splicing regulators, including SR proteins (SRSF11, SRSF12), RNA helicases (DDX26B, DDX6, DDX25), and Pre-mRNA processing factor (PRPF8), Splicing factor 3b (SF3B2). Conversely, HnRNPA3 and SF3B1 were downregulated. These findings suggest putrescine influences GnRH isoform expression through a dual mechanism: enhancing factors that promote alternative splicing while simultaneously attenuating components of the canonical splicing machinery. Our results provide novel insights into the molecular regulation of GnRH splicing and highlight putrescine as a potential modulator of reproductive function through alternative splicing mechanisms. - Source: PubMed
Publication date: 2025/04/11
Gautam PoojaSrivastava VijigishaBammidi SridharGhosh SayanBabu Vishnu SureshBanerjee Arnab - Oligo-astheno-teratozoospermia (OAT) is a common cause of male infertility, but the genetic basis of most OAT cases is still unknown. Here, one homozygous loss-of-function (LOF) variant in TDRD6, c.G1825T/p.Gly609X, was identified in an infertile patient with severe OAT by whole-exome sequencing (WES) and Sanger confirmation. Furthermore, Tdrd6-mutant mice (p.Gly615X; equivalent to p.Gly609X in human TDRD6) were generated. Remarkably, the Tdrd6-mutated mice mimicked the severe OAT symptoms of the patient. In addition, the architecture of chromatoid bodies (CBs) were disrupted in round spermatids from Tdrd6-mutant mice, leading to blocked spermatogenesis in the round spermatids. The assembly of PIWIL1, TDRD1, TDRD7 and DDX25 in CBs was disturbed in the Tdrd6-mutant mice. Applying immunoprecipitation-mass spectrometry (IP-MS), we identified some TDRD6-interacting partners, including CB proteins TDRD7, MAEL and PCBP1. Moreover, we described the assisted reproductive technology (ART) outcomes of the infertile patient and his partner. Altogether, our findings provide necessary evidences to support the idea that the homozygous LOF variant in TDRD6 induces male infertility with severe OAT, suggesting that TDRD6 could be a useful genetic diagnostic target for male infertility. - Source: PubMed
Bi XinyingJin HuijuanWan FengXia YanqingGuo HaibinChen SurenWang Binbin - Obesity, a chronic metabolic disorder, is related to cardiovascular diseases, diabetes, cancer, and reproductive disorders. The relationship between obesity and male infertility is now well recognized, but the mechanisms involved are unclear. We aimed to observe the effect of obesity on spermatogenesis and to investigate the role of histone ubiquitination and acetylation modifications in obesity-induced spermatogenesis disorders. - Source: PubMed
Publication date: 2024/04/17
Fofana MahamadouLi ZhenyangLi HanLi WenqiWu LuLu LuLiu Qizhan - Colour agnosia is a disorder that impairs colour knowledge (naming, recognition) despite intact colour perception. Previously, we have identified the first and only-known family with hereditary developmental colour agnosia. The aim of the current study was to explore genomic regions and candidate genes that potentially cause this trait in this family. For three family members with developmental colour agnosia and three unaffected family members CGH-array analysis and exome sequencing was performed, and linkage analysis was carried out using DominantMapper, resulting in the identification of 19 cosegregating chromosomal regions. Whole exome sequencing resulted in 11 rare coding variants present in all affected family members with developmental colour agnosia and absent in unaffected members. These variants affected genes that have been implicated in neural processes and functions (CACNA2D4, DDX25, GRINA, MYO15A) or that have an indirect link to brain function, development or disease (MAML2, STAU1, TMED3, RABEPK), and a remaining group lacking brain expression or involved in non-neural traits (DEPDC7, OR1J1, OR8D4). Although this is an explorative study, the small set of candidate genes that could serve as a starting point for unravelling mechanisms of higher level cognitive functions and cortical specialization, and disorders therein such as developmental colour agnosia. - Source: PubMed
Publication date: 2023/09/06
Nijboer Tanja C WHessel Ellen V Svan Haaften Gijs Wvan Zandvoort Martine Jvan der Spek Peter JTroelstra Christinede Kovel Carolien G FKoeleman Bobby P Cvan der Zwaag BertBrilstra Eva HBurbach J Peter H