Ddx4
- Known as:
- Ddx4
- Catalog number:
- 046160A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Ddx4
Related genes to: Ddx4
- Gene:
- DDX4 NIH gene
- Name:
- DEAD-box helicase 4
- Previous symbol:
- -
- Synonyms:
- VASA
- Chromosome:
- 5q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-05-30
- Date modifiied:
- 2016-10-05
Related products to: Ddx4
Related articles to: Ddx4
- As a member of the Groucho/TLE family, Transducin-like enhancer of split 3 (TLE3) functions as a transcriptional co-repressor that is highly expressed in the testis. It recruits histone deacetylases (HDACs) and binds histones to mediate chromatin remodeling, thereby regulating gene expression. To investigate the physiological function of TLE3 in spermatogenesis, we generated germ cell-specific conditional knockout (cKO) mouse models using Stra8-Cre and Vasa-Cre drivers. However, Tle3 cKO male mice exhibited grossly normal development and fertility. Histological examination revealed intact testicular architecture and normal spermatogenic progression in the knockout mice. Moreover, immunofluorescence analyses of key germ cell marker proteins, including DDX4 (pan-germ cell), PLZF (undifferentiated spermatogonia), c-Kit (differentiating spermatogonia), γH2AX (meiosis recombination initiation) and PNA (acrosome in spermatids), showed normal germ cell distribution and differentiation. Furthermore, TUNEL assays for apoptosis detection revealed no significant difference between control and cKO mice. Collectively, our findings demonstrate that TLE3 is dispensable for male germ cell development and spermatogenesis. - Source: PubMed
Publication date: 2026/06/17
Zhao YifanXu HaoranZhou ShuminYu ZiqiLiu DalinZhou HaoKe ShengweiSun Fei - Growth differentiation factor (GDF) 9 is a member of the transforming growth factor (TGF)-β superfamily, which plays an important role in mammalian ovarian follicular development and female fertility. However, its regulatory role in the male reproductive system remains largely unknown. - Source: PubMed
Jiang TiantuanGuo JinmingJiao YafeiXu MeinaHe JianLiu XiangyuQin GuangshengLiu XiaohongChen YaoshengCong PeiqingHe Zuyong - Identifying the origin of tumor-initiating ability is critical for targeted therapies. While early primordial germ cells (PGCs) inherently possess this ability, our previous study indicated that soma-to-PGC-like conversion (SPLC) facilitates its acquisition in mouse breast tumor cells. This study reports evidence of SPLC activation in the human hepatic tumor cell line HL7721, where tumor cells spontaneously exhibit sequential developmental stages, progressing from somatic tumor cells through intermediate stages to PGC-like and late germ cell-like stages. Knocking out PGC specification inducers (, , , or ) or fate-maintaining genes ( or ) suppressed both SPLC and tumor initiation. Collectively, our findings suggest that SPLC might be activated in human tumor cells, serving as a potential pathway for gaining tumor-initiating ability that involves human PGC-related pathways. These results demonstrate that the acquisition of PGC-like fate in somatic cells drives tumor malignant progression, providing a potential paradigm for targeted cancer therapy. - Source: PubMed
Publication date: 2026/06/04
Li JingZhang FengyuXiong JiLiu AipingLiu PeipeiMa ZhanLin Hui-KuanLiu Chunfang - Busulfan (Bus)-induced oligozoospermia still lacks a disease-modifying therapy, and its pathogenesis has been largely attributed to germ-cell DNA damage. Emerging evidence indicates that microbiota-derived metabolites are key determinants of spermatogenic failure. Saikosaponin A (SSA), a major triterpenoid from Bupleurum, has never been evaluated in male infertility. Consequently, its regulatory role in the gut microbiota-metabolite axis and causal efficacy remain completely undefined. - Source: PubMed
Publication date: 2026/06/09
Li YaqiuZhang BoqiHe GuitianShen CaomeihuiChang FuqiangYang JunjunWang SihuiWang YueyingZong JinxinLuo YuxinWang NanSun YananSui YueWu MengtingLu DongjinLi ChunjinZhou Xu - Asthma is a chronic respiratory disease affecting over 230 million people worldwide, with higher prevalence in women. Environmental allergens such as house dust mite (HDM) trigger airway inflammation and hyperresponsiveness (AHR), yet the epigenetic mechanisms underlying these responses remain poorly understood. Furthermore, the role of estrogen receptors in the context of asthma is understudied. We aimed to investigate whether estrogen receptor-specific DNA methylation contributes to HDM-induced airway remodeling and hyperresponsiveness. Male and female C57BL/6J wild-type mice and estrogen receptor α and β knockout mice (Esr1 and Esr2) were exposed to HDM or phosphate-buffered saline for five weeks. DNA methylation and RNA sequencing data were obtained from snap-frozen whole lung tissues. HDM exposure resulted in widespread differential methylation of genes associated with inflammation and AHR, including . Notably, the absence of estrogen receptor β (in Esr2 mice) produced the most pronounced methylation patterns, particularly in females. Pathway enrichment analysis revealed asthma-relevant processes such as extracellular matrix remodeling, leukocyte adhesion and migration, airway smooth muscle contraction, and inflammatory signaling. Integration of methylation and gene expression data confirmed significant correlations (p<0.05) for , , and , and a marginal correlation for Chst7 (p<0.1), implicating these genes in allergic asthma pathogenesis. Our findings demonstrate that HDM exposure induces sex-specific epigenetic changes mediated by estrogen receptor status, highlighting a potential mechanism for increased asthma susceptibility in women. These results can inform estrogen receptor-targeted treatment strategies for allergic airway diseases. - Source: PubMed
Publication date: 2026/06/12
Commodore SarahEkpruke Carolyn DamilolaAlford RachelBorges-Sosa Omar AlejandroRousselle DustinBabayev MaksatIgwe ChukwudikeHemmerich Christopher MRusch Douglas BSilveyra Patricia