Mouse polyclonal to MORG1, Host Mouse
- Known as:
- Mouse pab MORG1, Host Mouse
- Catalog number:
- YF-PA26722
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse polyclonal MORG1 Host
Related genes to: Mouse polyclonal to MORG1, Host Mouse
- Gene:
- WDR83 NIH gene
- Name:
- WD repeat domain 83
- Previous symbol:
- -
- Synonyms:
- MORG1
- Chromosome:
- 19p13.13
- Locus Type:
- gene with protein product
- Date approved:
- 2010-01-25
- Date modifiied:
- 2013-01-09
Related products to: Mouse polyclonal to MORG1, Host Mouse
Related articles to: Mouse polyclonal to MORG1, Host Mouse
- WDR83 (WD Repeat Domain 83), also known as MORG1 (Mitogen-activated protein kinase Organizer 1), functions as a scaffold protein regulating diverse cellular processes, including cell signaling, proliferation, protein degradation, cell polarity, and autophagy. Through whole-exome sequencing, we identified a novel de novo WDR83 variant [NM_001099737; c.653 T > C,p.(L218P)] in a Japanese female patient presenting with global developmental delay, intellectual disability, and dysmorphic features. As the p.L218P variant was suspected to exert a dominant-negative effect, we investigated its impact on neuronal development. In vivo, acute expression via in utero electroporation promoted premature cell cycle exit of neural stem cells, impaired cortical neuron migration, and disrupted dendritic arborization, whereas axonal projections to the contralateral hemisphere remained unaffected. Additionally, cortical neurons expressing WDR83-L218P exhibited reduced spine head diameter. In vitro, WDR83-L218P expression inhibited axon elongation in primary cultured hippocampal neurons. Collectively, these findings suggest that WDR83 is a novel gene associated with neurodevelopmental disorders. Based on expression profiles and functional analyses, we conclude that WDR83 plays a crucial role in regulating neuronal morphology during brain development, and that the p.L218P variant disrupts this function, contributing to the patient's phenotype. - Source: PubMed
Publication date: 2025/12/11
Tabata HidenoriHasegawa YuikoYanagi KumikoSugawara RyotaIto HidenoriNishi ErikoKaname TadashiOkamoto NobuhikoNagata Koh-Ichi - HTLV-1 is an oncovirus that encodes a transactivator Tax and a regulatory gene HBZ. HTLV-1 early or infectious replication depends on Tax; during HTLV-1 late infection, HBZ plays a crucial role in driving the proliferation of infected cells and maintaining viral persistence. The biphasic replication pattern of HTLV-1 dictated by Tax and HBZ represents a result of viral host adaptation, but how HTLV-1 coordinates Tax and HBZ expression to facilitate early and late infection remains elusive. Here we reveal that HBZ RNA splicing exhibits distinct patterns in Tax+ and Tax- HTLV-1 infected cells. We demonstrate that Tax interacts with the host spliceosome and inhibits HBZ splicing by competitively binding splicing factors including WDR83 and GPATCH1. As a result, Tax confers a natural constraint on HBZ, counterbalancing its anti-replication effect at HTLV-1 early infection, while unleashing HBZ to drive HTLV-1 mitotic propagation during late infection. The splicing-dependent restriction of HBZ by Tax thus represents a critical interplay central to HTLV-1 persistence. - Source: PubMed
Publication date: 2025/07/28
Liang YiLyu ChenyangXu ShuwenTan ChenxinJiang QianLiu BenquanYang SikaiHuang WeijiaZhou RuoningYuan XiaoyiZuo XiaoruiMatsuoka MasaoMa Guangyong - Pre-mRNA splicing plays a key role in the regulation of gene expression. Recent discoveries suggest that defects in pre-mRNA splicing, resulting from the dysfunction of certain splicing factors, can impact the expression of genes crucial for genome surveillance mechanisms, including those involved in cellular response to DNA damage. In this study, we analyzed how cells with a non-functional spliceosome-associated Gpl1-Gih35-Wdr83 complex respond to DNA damage. Additionally, we investigated the role of this complex in regulating the splicing of factors involved in DNA damage repair. Our findings reveal that the deletion of any component within the Gpl1-Gih35-Wdr83 complex leads to a significant accumulation of unspliced pre-mRNAs of DNA repair factors. Consequently, mutant cells lacking this complex exhibit increased sensitivity to DNA-damaging agents. These results highlight the importance of the Gpl1-Gih35-Wdr83 complex in regulating the expression of DNA repair factors, thereby protecting the stability of the genome following DNA damage. - Source: PubMed
Publication date: 2024/04/10
Cipakova IngridJurcik MatusSelicky TomasLalakova Laura OliviaJakubikova JanaCipak Lubos - Macroautophagy/autophagy is a conserved lysosomal degradation process composed of both selective and nonselective degradation pathways. The latter occurs upon nutrient depletion. Selective autophagy exerts quality control of damaged organelles and macromolecules and is going on also under nutrient-replete conditions. Proper regulation of autophagy is vital for cellular homeostasis and prevention of disease. During nutrient availability, autophagy is inhibited by the MTORC1 signaling pathway. However, selective, basal autophagy occurs continuously. How the MTORC1 pathway is fine-tuned to facilitate basal constitutive autophagy is unclear. Recently, we identified the WD-domain repeat protein WDR83/MORG1 as a negative regulator of MTORC1 signaling allowing basal, selective autophagy. WDR83 interacts with both the Ragulator and active RRAG GTPases to prevent recruitment of the MTORC1 complex to the lysosome. Consequently, WDR83 depletion leads to hyperactivation of the MTORC1 pathway and a strong decrease in basal autophagy. As a consequence of WDR83 depletion cell proliferation and migration increase and low levels of mRNA are correlated with poor prognosis for several cancers. - Source: PubMed
Publication date: 2024/03/07
Kournoutis AthanasiosLamark TrondJohansen TerjeAbudu Yakubu Princely - Somatic mutations contribute to cancer development by altering the activity of enhancers. In the study, a total of 135 mutation-driven enhancers, which displayed significant chromatin accessibility changes, were identified as candidate risk factors for breast cancer (BRCA). Furthermore, we identified four mutation-driven enhancers as independent prognostic factors for BRCA subtypes. In Her2 subtype, enhancer G > C mutation was associated with poorer prognosis through influencing its potential target genes FBXW9, TRIR, and WDR83. We identified aminoglutethimide and quinpirole as candidate drugs targeting the mutated enhancer. In normal subtype, enhancer G > A mutation was associated with poorer prognosis through influencing its target genes ALOX15B, LINC00324, and MPDU1. We identified eight candidate drugs such as erastin, colforsin, and STOCK1N-35874 targeting the mutated enhancer. Our findings suggest that somatic mutations contribute to breast cancer subtype progression by altering enhancer activity, which could be potential candidates for cancer therapy. - Source: PubMed
Publication date: 2024/01/05
Zhao HongyingFeng KeLei JunjieShu YaopengBo LinLiu YingWang LixiaLiu WangyangNing ShangweiWang Li