MIR608

Last update 08 May 2025

Basic Info

Synonyms

hsa-mir-608, microRNA 608, MIR608

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Introduction-

100 Clinical Results associated with MIR608

100 Translational Medicine associated with MIR608

0 Patents (Medical) associated with MIR608

112

Literatures (Medical) associated with MIR608

01 Jun 2025·Gene

Analyzing the role of genetic variants in microRNAs and its role as a modulator towards Chronic Obstructive Pulmonary disease (COPD) susceptibility in North Indian population

Article

Author: Garg, Kranti ; Bhatia, Anmol ; Chopra, Vishal ; Upadhyay, Atul Kumar ; Sharma, Siddharth

BACKGROUNDmiRNAs can target numerous genes, with slight expression changes potentially leading to significant alterations in protein-coding gene expression, affecting various biological processes and possibly worsening conditions like COPD.OBJECTIVESThis study examines the link between six miRNA SNPs (MIR605, MIR608, MIR3117, MIR149, MIR499, and MIR25) and COPD risk in a North Indian population and the functional impact of these miRNA-SNPs on COPD-related pathological factors.MATERIALS AND METHODSTo assess genotypes, a case-control study was conducted with 323 COPD cases and 350 hospital controls. Logistic regression determined the odds ratio and 95% confidence interval for the SNP-COPD association, with stratified analysis for clinical parameters, symptoms, and risk factors. SNP-SNP interactions were analyzed using combinatorial analysis, MDR, and CART analysis.RESULTSMIR25 SNP rs1527423 and MIR608 SNP rs4919510 were significantly associated with COPD risk (OR = 6.38; p < 0.0001 and OR = 1.43, p = 0.02, respectively). rs1527423 remained significant in stratified analysis for age (OR = 6.19; pc = 0.0005), gender (males; OR = 5.93; pc < 0.0001), and smoking status (smokers; OR = 5.02; pc = 0.0006). rs4919510 was associated with COPD risk in patients aged ≥ 65 years (OR = 2.38, pc = 0.0054). MIR605 SNP rs2043556 had a protective effect in non-smokers (OR = 0.142; pc = 0.048). MIR3117 SNP rs4655646 was linked to COPD symptoms. Doublet combinations of each SNP with rs1527423 increased COPD risk. CART analysis identified rs1527423 as a critical factor, with the genotypic combination of 149(M)-3117(M; W)-605(M; W)-608(M; H)-25(W) showing the highest COPD risk (OR = 11; p = 0.0445).CONCLUSIONSThe study suggests MIR25 SNP rs1527423 as a risk factor for COPD in North Indian populations.

12 Feb 2025·Combinatorial Chemistry & High Throughput Screening

Investigation of LncRNA Expression Profiles and Analysis of Immune-Related lncRNA-miRNA-mRNA Networks in Neovascular Age-Related Macular Degeneration

Article

Author: Gao, Xiang ; Lu, Xiuhai ; Liu, Wencai ; Tian, Jingyi ; Qin, Liying ; Yuan, Gongqiang

Introduction:Age-related Macular Degeneration (AMD) is a predominant cause of blindness in the elderly. The present study is the first to investigate the alteration of lncRNAs and mRNAs in neovascular AMD.Methods:Nine patients with neovascular AMD were included in the study. The control group comprised seven patients with epiretinal membranes. RNA sequencing was performed to obtain the differentially expressed mRNAs (DEmRNAs) and lncRNAs (DElncRNAs). Then, the DElncRNA-DEmRNA co-expression network, ceRNA network, and immune-related ceRNA subnetwork were constructed. Functional annotation of DEmRNAs between the two groups and DEmRNAs in networks was conducted. The immune cell distribution in neovascular AMD was also evaluated. Real-time qPCR (RT-qPCR) was used to validate the expression levels of key markers.Results:A total of 342 DEmRNAs and 157 DElncRNAs were obtained in neovascular AMD. Functional annotation indicated that these DEmRNAs significantly enriched immune systemrelated processes, such as positive regulation of B cell activation, immunoglobulin receptor binding, complement activation, and classical pathway. The DElncRNA-DEmRNA co-expression network, including 185 DElncRNA-DEmRNA co-expression pairs, and the ceRNA (DElncRNA-miRNA-DEmRNA) network, containing 45 lncRNA-miRNA pairs and 73 miRNAmRNA pairs, were constructed. The immune-related ceRNA subnetwork, including 2 lncRNAs, 5 miRNAs, and 3 mRNAs, was constructed. In addition, the distribution of immune cells was slightly different between the neovascular AMD group and the control group. RT-qPCR validation indicated the consistency between the RT-qPCR results and RNA sequencing results.Conclusion:In conclusion, STC1, S100A1, MEG3, MEG3-hsa-miR-608-S100A1, and MEG3- hsa-miR-130b-3p/hsa-miR-149-3p-STC1 may be related to the occurrence and development of neovascular AMD.

01 Dec 2024·Cellular and Molecular Life Sciences

Ribosomal protein L24 mediates mammalian microRNA processing in an evolutionarily conserved manner

Article

Author: Mishra, Nibha ; Soreq, Hermona ; Bennett, Estelle R ; Tzur, Yonat ; Bar, Adi ; Nadorp, Bettina ; Heppenstall, Paul ; Winek, Katarzyna ; Greenberg, David S ; Madrer, Nimrod ; Dubnov, Serafima

AbstractTo investigate the mechanism(s) underlying the expression of primate-specific microRNAs (miRs), we sought DNA regulatory elements and proteins mediating expression of the primate-specific hsa-miR-608 (miR-608), which is located in the SEMA4G gene and facilitates the cholinergic blockade of inflammation by targeting acetylcholinesterase mRNA. ‘Humanized’ mice carrying pre-miR-608 flanked by 250 bases of endogenous sequences inserted into the murine Sema4g gene successfully expressed miR-608. Moreover, by flanking miR-608 by shortened fragments of its human genome region we identified an active independent promoter within the 150 nucleotides 5′ to pre-miR-608, which elevated mature miR-608 levels by 100-fold in transfected mouse- and human-originated cells. This highlighted a regulatory role of the 5′ flank as enabling miR-608 expression. Moreover, pull-down of the 150-base 5′ sequence revealed its interaction with ribosomal protein L24 (RPL24), implicating an additional mechanism controlling miR-608 levels. Furthermore, RPL24 knockdown altered the expression of multiple miRs, and RPL24 immunoprecipitation indicated that up- or down-regulation of the mature miRs depended on whether their precursors bind RPL24 directly. Finally, further tests showed that RPL24 interacts directly with DDX5, a component of the large microprocessor complex, to inhibit miR processing. Our findings reveal that RPL24, which has previously been shown to play a role in miR processing in Arabidopsis thaliana, has a similar evolutionarily conserved function in miR biogenesis in mammals. We thus characterize a novel extra-ribosomal role of RPL24 in primate miR regulation.Graphical abstract

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