Ask about this productRelated genes to: CLRN1 antibody
- Gene:
- CLRN1 NIH gene
- Name:
- clarin 1
- Previous symbol:
- USH3, USH3A, RP61
- Synonyms:
- -
- Chromosome:
- 3q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-23
- Date modifiied:
- 2019-04-23
- Gene:
- CLRN1-AS1 NIH gene
- Name:
- CLRN1 antisense RNA 1
- Previous symbol:
- CLRN1OS
- Synonyms:
- UCRP
- Chromosome:
- 3q25.1
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2007-01-05
- Date modifiied:
- 2014-11-19
Related products to: CLRN1 antibody
Related articles to: CLRN1 antibody
- Lung cancer is one of the most common malignancies, characterized by a wide prognosis spectrum, different histological subtypes, and a high mortality rate. Hemostatic system imbalance in patients with lung cancer often leads to increased mortality. Intracellular RNAs that share common miRNA binding sites create a competing endogenous RNA (ceRNA) network that plays an important role in gene expression regulation. The emerging role of ceRNAs in tumor development is increasingly being recognized; however, their connection to hemostatic system imbalance in lung squamous cell carcinoma (LUSC) remains unclear. In this study, RNA-seq data of LUSC and normal tissues were downloaded from the TCGA data portal. Differentially expressed mRNAs (DEmRNAs), miRNAs (DEmiRNAs), and lncRNAs (DElncRNAs) between LUSC and corresponding paracancerous tissues were analyzed using the DESeq2 package in R statistical software. Hemostasis-related genes linked to coagulation and complement cascades (hsa04610) and platelet activation (hsa04611) pathways were identified using the KEGGREST package. The ceRNA network associated with system hemostasis was constructed using differentially expressed RNAs (DERNAs), including mRNAs, lncRNAs, and miRNAs. The GO and KEGG enrichment analysis of DEmRNAs was conducted using the enrichR package. Hazard ratio (HR) and Kaplan-Meier curve were employed to assess the prognostic value of DERNAs using the survival and survminer packages. A ceRNA network comprising 100 hemostasis-related genes, 5 miRNAs, and 57 lncRNAs was constructed. Of these, 19 hemostasis genes, one miRNA (miR-23-3p), and 6 lncRNAs (LINC01615, LINC00707, LINC00702, FEZF1-AS1, DLX6-AS1, CLRN1-AS1) were significantly associated with prognosis in LUSC. Based on correlation analysis, MEF2C-AS1/miR-429/F8, RAP1A, GNAI2, C3AR1, F13A1, P2RY12, LCP2, C1QC axis and CASC11, CASC9, PVT1, BBOX1-AS1/ miR-23b-3p/ PLAU axis may represent key pathways involved in hemostatic system imbalance and the pathogenesis of LUSC. Our analysis revealed a complex ceRNA network associated with system hemostasis and the prognosis of LUSC. These findings may contribute to the development of personalized therapies and valuable prognostic biomarkers for LUSC patients. - Source: PubMed
Publication date: 2025/12/17
Mirazimi YasinGharechahi Javad - Hepatocellular carcinoma (HCC), as a very aggressive and lethal tumor type, is a serious threat to human health. In the process of information exchange between tumor cells, studies focused on how CLRN1-AS1 inhibits the proliferation and migration of HCC cells by targeting the miR-320c/SRSF7 signaling pathway, and further analyzed its potential mechanism in HCC progression. In order to achieve the objective of this study, the exosomes of human liver cell line THLE-3 were cultured and isolated in vitro. Quantitative real-time polymerase chain reaction (RT-qPCR) was used to accurately detect the expression level of CLRN1-AS1. The proliferation and apoptosis of HCC cells were comprehensively analyzed by plate clone formation assay, EdU assay and TUNEL assay. The cell migration ability was evaluated by Transwell assay. In order to further explore the binding relationship between CLRN1-AS1 and miR-320c and its regulatory effect on SRSF7, subcell separation technology, RNA pull-down experiment, RNA immunoprecipitation (RIP) experiment and luciferase report experiment were used in this study. Western blot and nanoparticle tracking analysis (NTA) were used to further verify the above experimental results. The results showed that the secretion of CLRN1-AS1 in exosomes significantly inhibited the proliferation and migration of HCC cells. CLRN1-AS1 binds to miR-320c, which targets the expression of SRSF7. The experiment also showed that CLRN1-AS1 affects the proliferation, apoptosis and migration of HCC cells by regulating SRSF7. These findings are supported by cellular thermal and medical thermal imaging, providing a new perspective for decoding the intercellular thermal action. - Source: PubMed
Publication date: 2025/06/11
Hao GaopengXie ChanghuWang Yinquan - Tuberculosis (TB) is the leading cause of death among people with HIV-1 infection. To improve the diagnosis and treatment of HIV-TB patients, it is important to understand the mechanisms underlying these conditions. Here, we used an integrated genomics approach to analyze and determine the lncRNAs that are dysregulated in HIV-TB patients and HIV-TB patients undergoing anti-retroviral therapy (ART) using a dataset available in the public domain. The analyses focused on the portion of the genome transcribed into non-coding transcripts, which historically have been poorly studied and received less focus. This revealed that Mtb infection in HIV prominently up-regulates the expression of long non-coding RNA (lncRNA) genes , , , , and and down-regulates the expression of lncRNAs , , , , and . It also revealed that ART down-regulates the expression of some lncRNA genes (, , , and ) that are highly up-regulated in HIV-TB patients. Furthermore, the interrogation of the genomic regions that are associated with regulated lncRNAs showed enrichment for biological processes linked to immune pathways in TB-infected conditions. However, intriguingly, TB patients treated with ART showed completely opposite and non-overlapping pathways. Our findings suggest that lncRNAs could be used to identify critical diagnostic, prognostic, and treatment targets for HIV-TB patients. - Source: PubMed
Publication date: 2024/07/13
Reid Victoria ARamos Enrique IVeerapandian RajaCarmona AreannaGadad Shrikanth SDhandayuthapani Subramanian - Frailty is the most common medical condition affecting the aging population, and its prevalence increases in the population aged 65 or more. Frailty is commonly diagnosed using the frailty index (FI) or frailty phenotype (FP) assessments. Observational studies have indicated the association of frailty with Alzheimer's disease (AD). However, the shared genetic and biological mechanism of these comorbidity has not been studied. To assess the genetic relationship between AD and frailty, we examined it at single nucleotide polymorphism (SNP), gene, and pathway levels. Overall, 16 genome-wide significant loci (15 unique loci) ( < 5 × 10) and 22 genes (21 unique genes) were identified between AD and frailty using cross-trait meta-analysis. The 8 shared loci implicated 11 genes: , , , , , , , , , , and between AD and FI, and 8 shared loci between AD and FFS implicated 11 genes: , , , , , , , , , , and . The loci 4p16.3 () was identified in both meta-analyses. The colocalization analysis supported the results of our meta-analysis in these loci. The gene-based analysis revealed 80 genes between AD and frailty, and 4 genes were initially identified in our meta-analyses: , , , and . The pathway analysis showed enrichment for lipoprotein particle plasma, amyloid fibril formation, protein kinase regulator, and tau protein binding. Overall, our results provide new insights into the genetics of AD and frailty, suggesting the existence of non-causal shared genetic mechanisms between these conditions. - Source: PubMed
Publication date: 2024/04/19
Enduru NiteshFernandes Brisa SZhao Zhongming - Trophoblast cells play an important role in embryo recognition and localization, as well as placental development during embryo implantation. Dysfunction of trophoblastic cells causes pathological changes that lead to insufficient recognition, positioning, and adhesion during embryo implantation, ultimately leading to embryo development has stopped. - Source: PubMed
Publication date: 2023/07/16
Zhang YueChen YingJiaoZhang LinyuWu YiLunFeng YingMa Fang