Ask about this productRelated genes to: ROPN1L Blocking Peptide
- Gene:
- ROPN1L NIH gene
- Name:
- rhophilin associated tail protein 1 like
- Previous symbol:
- -
- Synonyms:
- ASP, FLJ25776, RSPH11
- Chromosome:
- 5p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-05
- Date modifiied:
- 2016-10-05
Related products to: ROPN1L Blocking Peptide
Related articles to: ROPN1L Blocking Peptide
- (), the causative agent of enzootic pneumonia, disrupts mucociliary clearance by adhering to porcine ciliated airway cells, contributing to chronic respiratory disease. Traditional submerged cell cultures lack airway-like polarity and structural complexity, limiting studies. This study utilized a porcine air-liquid interface porcine respiratory epithelial cell (ALI-PREC) model to investigate infection dynamics, cytopathic effects (CPEs), and host-specific responses. Primary tracheal epithelial cells isolated from three 6-week-old pigs were cultured under air-liquid interface conditions for 4 weeks to form differentiated pseudostratified, ciliated epithelium. ALI-PRECs were inoculated with strain 232 at 10, 10, and 10 CCU/mL for 2 or 5 h and monitored for 144 h. Quantitative microscopy assessed total particle count, area, average size, and percentage area covered by particles, normalized against mock controls. adhered within 2 h, inducing CPE (cell rounding, clustering, and detachment) and reducing ciliary activity in a dose- and time-dependent manner. DNA was detected in the epithelium by 24 h post-inoculation (hpi) and in subnatants at higher doses, demonstrating epithelial barrier disruption. Ciliary beating persisted in some replicates, suggesting interindividual variability in host responses. Friis medium had no detectable impact on ALI-PRECs, validating its suitability for infection studies. Gene expression analysis revealed downregulation of ciliary motility genes (, , , and ) at 72 hpi and upregulation of intercellular junction genes (, , and ) by 120 hpi, suggesting a wound healing response. The ALI-PREC model effectively mirrors key aspects of pathogenesis, providing a robust platform for studying host-pathogen interactions and identifying therapeutic targets.IMPORTANCEDespite its economic impact on pigs, the mechanisms by which () causes enzootic pneumonia remain poorly understood. Early infection events (bacterial exposure and adherence) are hard to study because traditional cell cultures lack airway complexity and cellular diversity. We developed an model replicating porcine airway structure and cell populations. Using this model, we showed that rapidly adheres to airway cells and disrupts ciliary function and epithelial integrity in a dose- and time-dependent manner. These effects coincide with altered expression of genes governing ciliary motility and cell-cell junctions. Importantly, our model revealed natural variability in cytopathic responses among pigs, indicating that host-specific factors influence disease progression. These insights may guide personalized strategies for preventing and treating swine respiratory infections. - Source: PubMed
Publication date: 2026/06/18
Castillo-Espinoza Ana FNelli Rahul KMora-Díaz Juan CZhang DanyangRauh RolfReddi Bala MSaxena ApoorvaTwu Ning-ChiehEspin-Palazón RaquelGiménez-Lirola Luis G - Cilia are microtubule-based organelles essential for motility, sensory signaling and development. In humans, motile cilia facilitate fluid movement, and their dysfunction causes ciliopathies, including infertility. We used RNAi-mediated knockdown of two human spermatid flagellar genes in to assess effects on ciliary function and locomotion. Knockdown of and significantly reduced planarian swim rate by 26.4% and 33.2% respectively and shortened cilia by 37.1% and 38.7% respectively. These findings highlight the critical roles of ROPN1L and TEX9 in cilia function and the use of planarians as a valuable model for studying ciliopathies. . - Source: PubMed
Publication date: 2026/04/16
Pitt RachelGogoi ChayanikaCalnan AngelinaPatnaik LataJohnson Kristen C - Spermiogenesis requires extensive molecular and structural remodeling to produce motile sperm. Mutations in the testis-specific RNA methyltransferase NSUN7 are associated with defective fibrous sheath, impaired sperm motility, and male infertility. However, the underlying molecular mechanisms remain poorly understood. Here, we performed proteomic profiling of sorted, elongated, and round spermatids, as well as mature spermatozoa from Nsun7 knockout mice. We showed that NSUN7 is present at all stages of spermiogenesis and is most abundant in round spermatids, which corresponds to the formation of the flagellum and fibrous sheath assembly. Loss of NSUN7 altered the abundance of proteins essential for dynein arm assembly (PIH1D3, CCDC103, CCDC40), intraflagellar transport (IFT122), and fibrous sheath organization (AKAP3, AKAP4, ROPN1L). We also showed that the previously detected impaired retention of cytoplasm in elongated spermatids may be caused by plectin accumulation. Interestingly, no statistically significant changes were found in mature sperm proteomes upon Nsun7 inactivation. Our findings support a model in which NSUN7 primarily stabilizes protein complexes and coordinates flagellar assembly. This indicates that NSUN7 is a critical regulator of spermiogenesis, and its malfunction is a contributing factor to male infertility. - Source: PubMed
Publication date: 2025/12/25
Buev Vitaly SGuseva Ekaterina ARubtsova Maria PPriymak Anastasia VNovikova Svetlana EAverina Olga APermyakov Oleg AGrigoryeva Olga OManskikh Vasily NZgoda Victor GDontsova Olga ASergiev Petr V - BACKGROUND Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with limited effective treatments and significant challenges in early diagnosis. Identifying reliable biomarkers is crucial for improving diagnostic accuracy and patient outcomes. MATERIAL AND METHODS We analyzed TRIM family gene expression in IPF patients and healthy controls using GSE93606, GSE33566, and GSE38958 datasets. Consensus clustering and WGCNA identified IPF subtypes and hub genes. Machine learning models (RF, GLM, SVM, XGB) were built to identify key disease genes. A nomogram for clinical prediction was developed and validated. Peripheral blood samples from IPF patients and healthy controls were used to validate gene expression via qPCR. RESULTS TRIM family genes were significantly differentially expressed between IPF patients and healthy controls. Two distinct IPF subtypes (C1 and C2) were identified, each exhibiting unique biological functions and signaling pathways. The RF model outperformed other machine learning models, identifying TNIK, NCL, ROPN1L, MTR, and HNRNPH1 as key disease-characteristic genes. The nomogram demonstrated good predictive accuracy (AUC: 0.741, 95% CI: 0.556-0.897). qPCR validation confirmed increased expression of 4 genes in IPF patients, except for ROPN1L, which showed decreased expression. CONCLUSIONS This study identifies and validates TRIM family genes as potential biomarkers for IPF diagnosis using clinical samples. The findings support the integration of these biomarkers into diagnostic workflows, potentially enhancing early diagnosis and personalized treatment strategies for IPF patients. Further research is needed to explore the prognostic value and underlying mechanisms of these genes. - Source: PubMed
Publication date: 2025/06/20
Huang XiangfeiYu WenHua FuzhouWei AipingWang XifengChen Shibiao - Airway mucus hypersecretion is a prominent pathophysiological characteristic observed in chronic obstructive pulmonary disease (COPD), cystic fibrosis, and asthma. It is a significant risk factor for lung dysfunction and impaired quality of life. Therefore, it is crucial to investigate changes in the major genes expressed in the lungs during airway mucus hypersecretion. Such investigations can help to identify genetic targets for the development of effective treatments to manage airway mucus hypersecretion and improve clinical outcomes for those affected by these respiratory disorders. - Source: PubMed
Liu YulinLiu TingtingRuan LingZhu DanliHe YijingJia JingChen Yirong