ODAD3

Last update 08 May 2025

Basic Info

Synonyms

CCDC151, Coiled-coil domain-containing protein 151, MGC20983

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Introduction

Component of the outer dynein arm-docking complex (ODA-DC) that mediates outer dynein arms (ODA) binding onto the doublet microtubule (PubMed:25192045). Involved in mediating assembly of both ODAs and their axonemal docking complex onto ciliary microtubules (PubMed:25192045).

100 Clinical Results associated with ODAD3

100 Translational Medicine associated with ODAD3

0 Patents (Medical) associated with ODAD3

Literatures (Medical) associated with ODAD3

01 Feb 2024·Environmental Toxicology

Integrated analysis of single‐cell sequencing and weighted co‐expression network identifies a novel signature based on cellular senescence‐related genes to predict prognosis in glioblastoma

Article

Author: Yu, Xuebin ; Qi, Xuchen ; Bao, Qingquan

AbstractBackgroundGlioblastoma (GBM) is a highly aggressive cancer with heavy mortality rates and poor prognosis. Cellular senescence exerts a pivotal influence on the development and progression of various cancers. However, the underlying effect of cellular senescence on the outcomes of patients with GBM remains to be elucidated.MethodsTranscriptome RNA sequencing data with clinical information and single‐cell sequencing data of GBM cases were obtained from CGGA, TCGA, and GEO (GSE84465) databases respectively. Single‐sample gene set enrichment analysis (ssGSEA) analysis was utilized to calculate the cellular senescence score. WGCNA analysis was employed to ascertain the key gene modules and identify differentially expressed genes (DEGs) associated with the cellular senescence score in GBM. The prognostic senescence‐related risk model was developed by least absolute shrinkage and selection operator (LASSO) regression analyses. The immune infiltration level was calculated by microenvironment cell populations counter (MCPcounter), ssGSEA, and xCell algorithms. Potential anti‐cancer small molecular compounds of GBM were estimated by “oncoPredict” R package.ResultsA total of 150 DEGs were selected from the pink module through WGCNA analysis. The risk‐scoring model was constructed based on 5 cell senescence‐associated genes (CCDC151, DRC1, C2orf73, CCDC13, and WDR63). Patients in low‐risk group had a better prognostic value compared to those in high‐risk group. The nomogram exhibited excellent predictive performance in assessing the survival outcomes of patients with GBM. Top 30 potential anti‐cancer small molecular compounds with higher drug sensitivity scores were predicted.ConclusionCellular senescence‐related genes and clusters in GBM have the potential to provide valuable insights in prognosis and guide clinical decisions.

01 May 2023·Genetics in Medicine

Pathogenic variants in CLXN encoding the outer dynein arm docking–associated calcium-binding protein calaxin cause primary ciliary dyskinesia

Article

Author: Omran, Heymut ; Dougherty, Gerard W ; Honecker, Barbara I ; Olbrich, Heike ; Bracht, Diana ; Poeta, Marco ; Schwartz, Oliver ; Nöthe-Menchen, Tabea ; Keller, Ulrike ; Diderich, Karin E M ; Aprea, Isabella ; Nüsse, Harald ; Raidt, Johanna ; Hjeij, Rim ; Santamaria, Francesca ; Vogelberg, Christian

PURPOSEPrimary ciliary dyskinesia (PCD) is a heterogeneous disorder that includes respiratory symptoms, laterality defects, and infertility caused by dysfunction of motile cilia. Most PCD-causing variants result in abnormal outer dynein arms (ODAs), which provide the generative force for respiratory ciliary beating and proper mucociliary clearance.METHODSIn addition to studies in mouse and planaria, clinical exome sequencing and functional analyses in human were performed.RESULTSIn this study, we identified homozygous pathogenic variants in CLXN (EFCAB1/ODAD5) in 3 individuals with laterality defects and respiratory symptoms. Consistently, we found that Clxn is expressed in mice left-right organizer. Transmission electron microscopy depicted ODA defects in distal ciliary axonemes. Immunofluorescence microscopy revealed absence of CLXN from the ciliary axonemes, absence of the ODA components DNAH5, DNAI1, and DNAI2 from the distal axonemes, and mislocalization or absence of DNAH9. In addition, CLXN was undetectable in ciliary axonemes of individuals with defects in the ODA-docking machinery: ODAD1, ODAD2, ODAD3, and ODAD4. Furthermore, SMED-EFCAB1-deficient planaria displayed ciliary dysmotility.CONCLUSIONOur results revealed that pathogenic variants in CLXN cause PCD with defects in the assembly of distal ODAs in the respiratory cilia. CLXN should be referred to as ODA-docking complex-associated protein ODAD5.

01 Jan 2023·American journal of cancer research

Identification of hub genes associated with head and neck squamous cell carcinoma by integrated bioinformatics approach and RNA-seq validation analysis.

Article

Author: Shabeer, Amir ; Al-Qahtani, Wahidah H ; Gul, Jaweria ; Abdel-Maksoud, Mostafa A ; Aufy, Mohammed ; Mustafa, Sara ; Chandio, Khushboo ; Almutairi, Saeedah Musaed ; Bukhari, Rimsha Sadia ; Khan, Nazima Yousaf

Head and neck squamous cell carcinoma (HNSC) is one of the most lethal malignancies around the globe. Due to its complex nature, the diagnostic and prognostic signatures of HNSC remain poorly understood. This study was launched to identify signature genes and their signaling pathways related to the development of HNSC. In the current study, we retrieved the GSE53819 dataset from the Gene Expression Omnibus (GEO) database to determine the differentially expressed genes (DEGs) using the "Limma" R package. Adjusted P values P < 0.05 and |logFC| ≥ 1 were selected as the filtering conditions. To identify hub genes, the protein-protein interaction (PPI) network construction of the DEGs was performed using STRING. We further used UALCAN, GEPIA, OncoDB, GENT2, MEXPRESS, and HPA databases for the expression, validation, survival, and methylation analyses of the hub genes. The cBioPortal tool was used to investigate the genetic alterations in hub genes. CancerSEA, TIMER, DAVID, ENCORI, and DrugBank were also used to explore a few more hub gene-associated parameters. Lastly, HOK, FaDu, and SCC25 cell lines were used to validate hub gene expression via RNA sequencing (RNA-seq) technique. A total of top 250 DEGs were selected for detailed analysis in this study. From these DEGs, prognostic and diagnostic associated four hub genes, which could serve as potential molecular biomarkers and therapeutic targets in HNSC patients were identified. Four hub genes, including down-regulated DNAH1 and DNALI1, while up-regulated DNAH9 and CCDC151 were strongly implicated in HNSC. We also validated the same expression pattern of the hub genes using RNA-seq analysis in HNSC and normal cell lines. Moreover, this study also revealed some novel links between DNAH1, DNALI1, DNAH9, and CCDC151 expression and genetic alterations, promoter methylation status, immune cell infiltration, miRNAs, gene enrichment terms, and various chemotherapeutic drugs. In conclusion, we indicated four hub genes (DNAH1, DNALI1, DNAH9, and CCDC151) and their associated signaling pathways, which may improve our understanding of HNSC and could be used as new therapeutic targets.

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ODAD3

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