Ask about this productRelated genes to: MOV10L1 antibody
- Gene:
- MOV10L1 NIH gene
- Name:
- Mov10 like RISC complex RNA helicase 1
- Previous symbol:
- -
- Synonyms:
- DJ402G11.8, DKFZp434B0717, CHAMP
- Chromosome:
- 22q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-31
- Date modifiied:
- 2018-06-07
Related products to: MOV10L1 antibody
Related articles to: MOV10L1 antibody
- The formation of biomolecular condensates, such as Yb bodies in Drosophila ovarian somatic cells, is significantly contributed to by phase separation of scaffold proteins. Client proteins transiently accumulate via interactions with these scaffolds; however, how client flux is regulated remains unclear. Here, we investigate Shutdown, a client protein of Yb bodies-the site of Piwi-piRNA-induced silencing complex (piRISC) precursor (pre-Piwi-piRISC) formation-and show that cytosolic Shutdown connects Armitage and Piwi to promote Piwi deposition into Yb bodies before quickly returning to the cytosol. This return allows Armitage to transfer pre-Piwi-piRISC to mitochondria for maturation. Shutdown's acidic N terminus mediates self-repulsion, conferring its transient residence within Yb bodies. A point mutation in armitage, analogous to a human armitage/MOV10L1 mutation associated with azoospermia, traps Shutdown in Yb bodies, blocking Piwi-piRISC generation. This study reveals the mechanism underlying Shutdown's transient localization in Yb bodies and its essential role in Piwi-piRISC biogenesis and fertility. - Source: PubMed
Hirakata ShigekiFukaya TakashiFujita AoiKosako HidetakaSiomi Mikiko C - Splenic nodules in dogs that were historically classified under the broad term "fibrohistiocytic nodules" are now recognised as distinct entities within likely a biological continuum. These include lymphoid hyperplasia extending to indolent lymphoma and complex hyperplasia to stromal sarcoma. However, the molecular mechanisms underpinning these proposed progressions remain largely unexplored, particularly at the genomic and transcriptomic levels. This study aimed to delineate and compare the transcriptomic landscapes of four distinct canine splenic nodules through differential gene expression profiling. RNA sequencing was performed on twelve formalin-fixed, paraffin-embedded (FFPE) splenic tissue samples obtained from dogs diagnosed with lymphoid hyperplasia, complex hyperplasia, histiocytic sarcoma, and stromal sarcoma, with normal canine spleen serving as a control tissue. Comparative transcriptomic analysis identified 47 differentially expressed genes (DEGs) between splenic nodules and normal spleen, including , , , , , , , , , , and . Furthermore, 39 DEGs were significantly altered among the four splenic lesion types, such as , , , , , , , , , , , , , and . Many of these genes have previously been implicated in tumorigenesis and metastasis in other malignancies. These findings suggest that dysregulated gene expression may contribute to the activation of stromal cells and macrophages within the spleen, facilitating malignant transformation. Overall, these findings deliver novel transcriptomic insights into canine splenic tumorigenesis that may improve diagnostic precision, inform prognostic assessment, and support the development of targeted therapeutic strategies in veterinary oncology. - Source: PubMed
Publication date: 2026/01/29
Spröhnle-Barrera CleideAllavena RachelPalmieri Chiara - Male infertility, accounting for approximately 50% of global infertility cases, is a growing concern in reproductive medicine. A fundamental cause lies in disrupted spermatogenesis-a complex, highly regulated process involving mitotic proliferation, meiotic division, and spermiogenic remodeling. Among the key regulatory pathways, PIWI-interacting RNAs (piRNAs) and their associated PIWI proteins have emerged as essential players in maintaining germline genome integrity and ensuring successful sperm development. However, their clinical relevance remain underexplored. This review provides a comprehensive synthesis of the piRNA pathway's multifaceted roles across the full spectrum of spermatogenesis. We describe how piRNAs, together with PIWI proteins, silence transposable elements (TEs), guide chromatin remodeling, regulate mRNA translation, and protect sperm from environmental insults. We detail the stage-specific functions of piRNA machinery during spermatocytogenesis, spermatidogenesis, and spermiogenesis, supported by evidence from gene knockout models and cross-species studies. Particular emphasis is placed on piRNA biogenesis, including the primary processing pathway, the ping-pong amplification cycle, and terminal modifications mediated by enzymes such as PNLDC1 and TDRKH. Genetic disruptions in key piRNA pathway genes-including , , , and -have been linked to clinical phenotypes such as non-obstructive azoospermia and severe oligozoospermia. We explore how these mutations impair piRNA maturation, compromise TE silencing, and trigger germ cell arrest, highlighting their diagnostic and therapeutic relevance. In addition, we discuss emerging applications of piRNAs as non-invasive biomarkers in seminal plasma, with altered piRNA profiles correlating with reduced sperm count and motility. Beyond pathogenesis, the piRNA pathway presents a promising frontier for reproductive interventions. We examine translational strategies targeting piRNA-associated proteins (e.g., RNF8-MIWI interaction modulators) and the potential for piRNA-guided gene silencing in germ cells. Moreover, we consider the impact of environmental toxins and epigenetic stressors on piRNA dynamics, suggesting new angles for fertility preservation. In summary, this review positions the piRNA pathway as a central regulator of male reproductive health. By integrating molecular biology with clinical genetics, we provide a roadmap for leveraging piRNA biology in the diagnosis, management, and treatment of male infertility. - Source: PubMed
Publication date: 2025/09/22
Hong ZhidanHuang SihanLi LiGao YingMa BinyuFan QigangZhang YuanzhenWang Mei - Prolonged exposure to high temperatures and humidity can trigger heat stress in animals, leading to subsequent immune suppression. Lipopolysaccharides (LPSs) act as upstream regulators closely linked to heat stress, contributing to their immunosuppressive effects. After an initial examination of transcriptome sequencing data from individual samples, 48 genes displaying interactions were found to potentially be associated with heat stress. Subsequently, to delve deeper into this association, we gathered chicken bone marrow dendritic cells (BMDCs). We combined heat stress with lipopolysaccharides and utilized a 48 × 48 Fluidigm IFC quantitative microarray to analyze the patterns of gene changes under various treatment conditions. The results of the study revealed that the combination of heat stress and LPSs in a coinfection led to reduced expressions of , , and . These differentially expressed genes triggered a pro-inflammatory response within cells via the MAPK and IL-17 signaling pathways. This response, in turn, affected the intensity and duration of inflammation when experiencing synergistic stimulation. Therefore, LPSs exacerbate the immunosuppressive effects of heat stress and prolong cellular adaptation to stress. The combination of heat stress and LPS stimulation induced a cellular inflammatory response through pathways involving cAMP, IL-17, MAPK, and others, consequently leading to decreased expression levels of , , and . - Source: PubMed
Publication date: 2024/02/06
Yang GuangZhou XinyiChen ShutaoLiu AnfangLiu LingbinWang HaiweiWang QiguiLan Xi - Alzheimer's disease (AD) is a complex, and multifactorial neurodegenerative disease. Previous studies have revealed that oxidative stress, synaptic toxicity, autophagy, and neuroinflammation play crucial roles in the progress of AD, however, its pathogenesis is still unclear. Recent researches have indicated that ferroptosis, an iron-dependent programmed cell death, might be involved in the pathogenesis of AD. Therefore, we aim to screen correlative ferroptosis-related genes (FRGs) in the progress of AD to clarify insights into the diagnostic value. Interestingly, we identified eight FRGs were significantly differentially expressed in AD patients. 10,044 differentially expressed genes (DEGs) were finally identified by differential expression analysis. The following step was investigating the function of DEGs using gene set enrichment analysis (GSEA). Weight gene correlation analysis was performed to explore ten modules and 104 hub genes. Subsequently, based on machine learning algorithms, we constructed diagnostic classifiers to select characteristic genes. Through the multivariable logistic regression analysis, five features (RAF1, NFKBIA, MOV10L1, IQGAP1, FOXO1) were then validated, which composed a diagnostic model of AD. Thus, our findings not only developed genetic diagnostics strategy, but set a direction for further study of the disease pathogenesis and therapy targets. - Source: PubMed
Publication date: 2022/09/28
Deng YanyaoFeng YanjinLv ZhichengHe JinliChen XunWang ChenYuan MingyangXu TingGao WenzheChen DongjieZhu HongweiHou Deren