Ask about this productRelated genes to: WDR18 antibody
- Gene:
- WDR18 NIH gene
- Name:
- WD repeat domain 18
- Previous symbol:
- -
- Synonyms:
- Ipi3
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-10
- Date modifiied:
- 2015-08-26
Related products to: WDR18 antibody
Related articles to: WDR18 antibody
- Integrin β4 (gene name: ITGB4) overexpression is associated with aggressive phenotypes and poor prognosis across multiple solid tumors. Despite its clinical significance, therapeutic strategies targeting integrin β4 remain underdeveloped. Targeted protein degradation technology, particularly molecular glue degraders, offer a promising approach for eliminating oncoproteins. However, the serendipitous discovery of molecular glues and limited exploration of substrate receptor have largely hindered the rational development of molecular glue degraders. In this study, through high throughput screening from a natural product library, we identified halofuginone (HF) as a potential molecular glue that promotes integrin β4 degradation via the CRL4B E3 ubiquitin ligase complex. HF administration markedly disrupted the aggressive progression of tumor cell both in vitro and in vivo. In summary, our study not only establishes HF as a promising degrader of integrin β4 but also demonstrates the utility of natural product screening for discovering molecular glue degraders, providing a novel therapeutic strategy for targeting oncogenic transmembrane proteins. - Source: PubMed
Publication date: 2026/03/24
Gong WeiYang DiTian JunruiChai YufeiYu TiantianWu QingnanWang YanZhang WeiminZhan Qimin - The mismatch between the rapid expansion of breeding scale and outdated techniques has hindered the development of the sea cucumber () industry. Our previous work revealed that ecological seedling breeding can produce red-colored , a phenotype not observed in traditional artificial breeding, where individuals are typically green. To investigate the molecular and genetic basis of this novel red coloration, we compared the growth conditions of red sea cucumbers and green sea cucumbers, as well as the differences in the pigment composition, gene expression and metabolites of their body walls. Red individuals showed higher body length and weight, and elevated levels of astaxanthin, lutein, canthaxanthin, and β-carotene in the body wall. Transcriptomic and metabolomic analyses identified differentially expressed genes and metabolites associated with pigmentation. In particular, and , involved in the cytochrome P450 drug metabolism pathway, were significantly upregulated in red individuals and are known to play roles in pigment biosynthesis and light signal perception. Key metabolites such as astaxanthin and fucoxanthin were implicated in body color formation. Moreover, genes in the arachidonic acid metabolism pathway were highly expressed, suggesting that dietary factors may contribute to pigment synthesis and accumulation. These findings provide novel insights into the mechanisms underlying body color variation in and offer potential for improved breeding strategies. - Source: PubMed
Publication date: 2025/07/17
Han LingshuHao PengfeiXiao HaoranLi WeiyanFan YichenTian WanrongTian YeWang LuoChang YaqingDing Jun - This study was aimed at assessing the diagnostic utility of whole genome sequence analysis in a well-characterised research cohort of individuals referred with a clinical suspicion of Cornelia de Lange syndrome (CdLS) in whom prior genetic testing had not identified a causative variant. Short-read whole genome sequencing was performed on 195 individuals from 105 families, 108 of whom were affected. 100/108 of the affected individuals had prior relevant genetic testing, with no pathogenic variant being identified. The study group comprised 42 trios in which both parental samples were available for testing (42 affected individuals and 126 unaffected parents), 61 singletons (unrelated affected individuals), and two families with more than one affected individual. The results showed that 32 unrelated probands from 105 families (30.5%) had likely causative coding region-disrupting variants. Four loci were identified in > 1 proband: (10), (6), (3), and (2). Single variants were detected in the remaining genes (, , , , , , , , , , and ). Possibly causative variants in noncoding regions of were identified in four individuals. Single de novo variants were identified in five genes not previously reported to be associated with any developmental disorder: , , , , and . The clustering of de novo noncoding variants implicates a single upstream open reading frame (uORF) and a small region in Intron 21 in regulation. Causative variants in genes encoding chromatin-associated proteins, with no defined influence on cohesin function, appear to result in CdLS-like clinical features. This study demonstrates the clinical utility of whole genome sequencing as a diagnostic test in individuals presenting with CdLS or CdLS-like phenotypes. - Source: PubMed
Publication date: 2025/01/30
Ansari MoradHalachev MihailParry DavidCampos Jose LD'Souza Elston NBarnett ChristopherWilkie Andrew O MBarnicoat AngelaPatel Chirag VSukarova-Angelovska ElenaGirisha Katta MFirth Helen VPrescott KatrinaWilson Louise CMcEntagart MerielDavidson RosemarieLynch Sally AnnJoss ShelaghHolden Simon TLam Wayne KSisodiya Sanjay MGreen Andrew JPoke GemmaWhiffin NicolaFitzPatrick David RMeynert Alison - Rixosome is a conserved, multi-subunit protein complex that has critical roles in ribosome biogenesis and silencing of Polycomb target genes. The subunits of human rixosome include PELP1, WDR18, TEX10, LAS1L and NOL9, with LAS1L providing the endoribonuclease activity and NOL9 the RNA 5' kinase activity. We report here cryo-EM structures of the human PELP1-WDR18-TEX10 and LAS1L-NOL9 complexes and a lower-resolution model of the human PELP1-WDR18-LAS1L complex. The structures reveal the overall organization of the human rixosome core scaffold of PELP1-WDR18-TEX10-LAS1L and indicate how the LAS1L-NOL9 endonuclease/kinase catalytic module is recruited to this core scaffold. Each TEX10 molecule has two regions of contact with WDR18, while the helix at the C terminus of WDR18 interacts with the helical domain of LAS1L. The structural observations are supported by our mutagenesis studies. Mutations in both WDR18-TEX10 contact regions can block the binding of TEX10, while truncation of the C-terminal helix of WDR18 can abolish the binding of LAS1L. The structures also reveal substantial conformational differences for TEX10 between the PELP1-WDR18-TEX10 complex alone and that in complex with pre-ribosome. - Source: PubMed
Publication date: 2025/04/07
Huang JiTong Liang - Comorbidity among atopic diseases (ADs) and gastrointestinal diseases (GIDs) has been repeatedly demonstrated by epidemiological studies, whereas the shared genetic liability remains largely unknown. Here we establish an atlas of the shared genetic architecture between 10 ADs or related traits and 11 GIDs, comprehensively investigating the comorbidity-associated genomic regions, cell types, genes and genetically predicted causality. Although distinct genetic correlations between AD-GID are observed, including 14 genome-wide and 28 regional correlations, genetic factors of Crohn's disease (CD), ulcerative colitis (UC), celiac disease and asthma subtypes are converged on CD4 T cells consistently across relevant tissues. Fourteen genes are associated with comorbidities, with three genes are known treatment targets, showing probabilities for drug repurposing. Lower expressions of WDR18 and GPX4 in PBMC CD4 T cells predict decreased risk of CD and asthma, which could be novel drug targets. MR unveils certain ADs led to higher risk of GIDs or vice versa. Taken together, here we show distinct genetic correlations between AD-GID pairs, but the correlated genomic loci converge on the dysregulation of CD4 T cells. Inhibiting WDR18 and GPX4 expressions might be candidate therapeutic strategies for CD and asthma. Estimated causality indicates potential guidance for preventing comorbidity. - Source: PubMed
Publication date: 2024/12/24
Qi CancanLi AnSu FengyuanWang YuZhou LongyuanTang CeFeng RuiMao RenChen MinhuChen LianminKoppelman Gerard HBourgonje Arno RZhou HongweiHu Shixian