| HGNC Family | Non-coding RNAs |
| Name | microRNA 6824 |
| 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": "\nThe collective evidence from these studies underscores that complement activation is a critical mediator of immune and inflammatory responses in multiple disease settings—including ocular degeneration, autoimmune disorders, and vascular, neural, and hepatic injuries. In this context, MIR6824 is proposed to function as a regulatory microRNA that fine‐tunes the complement cascade by modulating the expression of key complement components and receptors. Such regulation may affect the initiation and amplitude of complement activation, as exemplified by the pivotal roles of C3 activation and its cleavage fragments (e.g., C3a and C5a) in orchestrating inflammation, cellular recruitment, and subsequent tissue remodeling. This modulatory role is particularly relevant in conditions like age‐related macular degeneration, antiphospholipid syndrome, and other inflammatory pathologies where complement activity serves both damaging and protective functions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, several studies have demonstrated that complement-driven processes, such as anaphylatoxin signaling and localized complement synthesis, are essential for the modulation of adaptive immunity, ischemia–reperfusion injury, neurodegeneration, and tumor progression. By impacting these processes, MIR6824 may serve as an important posttranscriptional regulator that helps balance proinflammatory and tissue‐protective signals across varied pathological states. Through effects on the upstream generation of complement activation products, alterations in MIR6824 levels could influence the efficiency of immune cell recruitment, local cytokine production, and even the onset of complement‐dependent tissue regeneration."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFinally, the role of complement in processes as diverse as angiogenesis, tissue repair, and regulation of adaptive immune responses—as illustrated by studies in renal pathologies, ocular neovascularization, and systemic inflammatory conditions—suggests that MIR6824 could be a critical molecular switch that helps integrate these signals. By adjusting complement effector functions, MIR6824 may not only determine the balance between tissue damage and repair but also influence clinical outcomes in diseases such as periodontitis, stroke, and glaucoma. In this way, targeting MIR6824 or its downstream effects might provide new therapeutic avenues to modulate complement-driven pathology."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Y Han, T R Kozel, M X Zhang, et al. 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| Synonyms | HSA-MIR-6824 |
| NCBI Gene ID | 102465495 |
| API | |
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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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MIR6824 has 0 functional associations with biological entities spanning 0 categories () extracted from 0 datasets.
Click the + buttons to view associations for MIR6824 from the datasets below.
If available, associations are ranked by standardized value
| Dataset | Summary |
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