| HGNC Family | Non-coding RNAs |
| Name | microRNA 6511a-2 |
| Description | microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. miRNAs are transcribed by RNA polymerase II as part of capped and polyadenylated primary transcripts (pri-miRNAs) that can be either protein-coding or non-coding. The primary transcript is cleaved by the Drosha ribonuclease III enzyme to produce an approximately 70-nt stem-loop precursor miRNA (pre-miRNA), which is further cleaved by the cytoplasmic Dicer ribonuclease to generate the mature miRNA and antisense miRNA star (miRNA*) products. The mature miRNA is incorporated into a RNA-induced silencing complex (RISC), which recognizes target mRNAs through imperfect base pairing with the miRNA and most commonly results in translational inhibition or destabilization of the target mRNA. The RefSeq represents the predicted microRNA stem-loop. [provided by RefSeq, Sep 2009] |
| Summary |
{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRecent findings indicate that MIR6511A2 may serve as a key regulatory microRNA in the context of chronic obstructive pulmonary disease (COPD), a condition characterized by chronic inflammation predominantly affecting the small airways. Its dysregulation is proposed to influence the inflammatory response by modulating gene expression pathways that underlie immune cell activation and cytokine production."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n \nEmerging evidence suggests that the impact of MIR6511A2 is intertwined with the activities of several cell types central to COPD pathology, including neutrophils, macrophages, T lymphocytes, and bronchial epithelial cells. By potentially regulating the recruitment, survival, and activation of these cells, MIR6511A2 may contribute to the persistent inflammation and tissue remodeling that lead to the irreversible airflow limitation seen in COPD."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n \nOverall, these insights point to a functional role for MIR6511A2 as a molecular mediator in lung inflammation and remodeling. This positions MIR6511A2 as a promising candidate for further investigation, with the potential to serve both as a biomarker for disease progression and as a target for novel therapeutic strategies aimed at mitigating the chronic inflammatory milieu characteristic of COPD."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Wei-An Chang, Ming-Ju Tsai, Shu-Fang Jian, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Systematic analysis of transcriptomic profiles of COPD airway epithelium using next-generation sequencing and bioinformatics."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Int J Chron Obstruct Pulmon Dis (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.2147/COPD.S173206"}], "href": "https://doi.org/10.2147/COPD.S173206"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30127601"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30127601"}]}]}]}
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| Synonyms | HSA-MIR-6511A-2, MIR6511A-2 |
| NCBI Gene ID | 102466812 |
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| Predicted Functions |
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| Co-expressed Genes |
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| Expression in Tissues and Cell Lines |
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MIR6511A2 has 0 functional associations with biological entities spanning 0 categories () extracted from 0 datasets.
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If available, associations are ranked by standardized value
| Dataset | Summary |
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