MIR4747 Gene

HGNC Family Non-coding RNAs
Name microRNA 4747
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": "\nAlthough the provided body of literature primarily focuses on the molecular and physiological consequences of mutations in skeletal muscle ion channels—specifically the voltage‐gated sodium channel NaV1.4 and the CaV1.1 calcium channel—and their roles in disorders such as periodic paralysis, myotonia, muscular dystrophy, and even Huntington’s disease–related muscle adaptations"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ", none of these abstracts directly address or mention MIR4747. In these studies, the emphasis is placed on the impact of channel mutations—whether causing aberrant gating leading to leaky currents or altered channel expression—and the resulting perturbations in muscle excitability and metabolism."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nGiven that MIR4747 is not explicitly discussed, its potential role must be inferred from its general classification as a microRNA—a regulator of post‐transcriptional gene expression. MicroRNAs typically modulate a variety of biological pathways, and one might speculate that MIR4747 could influence the expression of proteins involved in ion channel function or muscle metabolism. However, these manuscripts do not provide experimental evidence linking MIR4747 to either the phenotypic expression of channelopathies or to adaptive muscle responses documented in the mouse models and patient studies."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn summary, while the compiled studies deliver substantial insight into the critical roles of NaV1.4 and CaV1.1 in diverse neuromuscular disorders—as well as the systemic and metabolic consequences of aberrant channel function"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": "—they do not provide any direct elucidation of MIR4747’s function. Thus, any functional contribution of MIR4747 to the regulatory networks implicated in these muscle channelopathies remains to be determined in future studies.\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "T Shirakawa, K Sakai, Y Kitagawa, et al. "}, {"type": "b", "children": [{"type": "t", "text": "A novel murine myotonia congenita without molecular defects in the ClC-1 and the SCN4A."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Neurology (2002)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1212/wnl.59.7.1091"}], "href": "https://doi.org/10.1212/wnl.59.7.1091"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12370472"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12370472"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Carole Hirn, George Shapovalov, Olivier Petermann, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Nav1.4 deregulation in dystrophic skeletal muscle leads to Na+ overload and enhanced cell death."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Gen Physiol (2008)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1085/jgp.200810024"}], "href": "https://doi.org/10.1085/jgp.200810024"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "18625851"}], "href": "https://pubmed.ncbi.nlm.nih.gov/18625851"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Fenfen Wu, Wentao Mi, Dennis K Burns, et al. "}, {"type": "b", "children": [{"type": "t", "text": "A sodium channel knockin mutant (NaV1.4-R669H) mouse model of hypokalemic periodic paralysis."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Clin Invest (2011)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1172/JCI57398"}], "href": "https://doi.org/10.1172/JCI57398"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "21881211"}], "href": "https://pubmed.ncbi.nlm.nih.gov/21881211"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Brooke Lucas, Tarek Ammar, Shiemaa Khogali, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Contractile abnormalities of mouse muscles expressing hyperkalemic periodic paralysis mutant NaV1.4 channels do not correlate with Na+ influx or channel content."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Physiol Genomics (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1152/physiolgenomics.00166.2013"}], "href": "https://doi.org/10.1152/physiolgenomics.00166.2013"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "24714718"}], "href": "https://pubmed.ncbi.nlm.nih.gov/24714718"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "Silvia Corrochano, Roope Männikkö, Peter I Joyce, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Novel mutations in human and mouse SCN4A implicate AMPK in myotonia and periodic paralysis."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Brain (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1093/brain/awu292"}], "href": "https://doi.org/10.1093/brain/awu292"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "25348630"}], "href": "https://pubmed.ncbi.nlm.nih.gov/25348630"}]}, {"type": "r", "ref": 6, "children": [{"type": "t", "text": "Fenfen Wu, Wentao Mi, Yu Fu, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Mice with an NaV1.4 sodium channel null allele have latent myasthenia, without susceptibility to periodic paralysis."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Brain (2016)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1093/brain/aww070"}], "href": "https://doi.org/10.1093/brain/aww070"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "27048647"}], "href": "https://pubmed.ncbi.nlm.nih.gov/27048647"}]}, {"type": "r", "ref": 7, "children": [{"type": "t", "text": "Silvia Corrochano, Gonzalo Blanco, Debbie Williams, et al. "}, {"type": "b", "children": [{"type": "t", "text": "A genetic modifier suggests that endurance exercise exacerbates Huntington's disease."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Hum Mol Genet (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1093/hmg/ddy077"}], "href": "https://doi.org/10.1093/hmg/ddy077"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "29509900"}], "href": "https://pubmed.ncbi.nlm.nih.gov/29509900"}]}, {"type": "r", "ref": 8, "children": [{"type": "t", "text": "Marino DiFranco, Stephen C Cannon "}, {"type": "b", "children": [{"type": "t", "text": "Voltage-dependent Ca"}, {"type": "a", "children": [{"type": "t", "text": "sup"}], "href": "sup"}, {"type": "t", "text": "2+"}, {"type": "a", "children": [{"type": "t", "text": "/sup"}], "href": "/sup"}, {"type": "t", "text": " release is impaired in hypokalemic periodic paralysis caused by Ca"}, {"type": "a", "children": [{"type": "t", "text": "sub"}], "href": "sub"}, {"type": "t", "text": "V"}, {"type": "a", "children": [{"type": "t", "text": "/sub"}], "href": "/sub"}, {"type": "t", "text": "1.1-R528H but not by Na"}, {"type": "a", "children": [{"type": "t", "text": "sub"}], "href": "sub"}, {"type": "t", "text": "V"}, {"type": "a", "children": [{"type": "t", "text": "/sub"}], "href": "/sub"}, {"type": "t", "text": "1.4-R669H."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Am J Physiol Cell Physiol (2022)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1152/ajpcell.00209.2022"}], "href": "https://doi.org/10.1152/ajpcell.00209.2022"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "35759432"}], "href": "https://pubmed.ncbi.nlm.nih.gov/35759432"}]}]}]}
Synonyms MIR-4747
NCBI Gene ID 100616337
API
Download Associations
Predicted Functions View MIR4747's ARCHS4 Predicted Functions.
Co-expressed Genes View MIR4747's ARCHS4 Predicted Functions.
Expression in Tissues and Cell Lines View MIR4747's ARCHS4 Predicted Functions.

Functional Associations

MIR4747 has 279 functional associations with biological entities spanning 3 categories (molecular profile, cell line, cell type or tissue, gene, protein or microRNA) extracted from 9 datasets.

Click the + buttons to view associations for MIR4747 from the datasets below.

If available, associations are ranked by standardized value

Dataset Summary
CCLE Cell Line Gene CNV Profiles cell lines with high or low copy number of MIR4747 gene relative to other cell lines from the CCLE Cell Line Gene CNV Profiles dataset.
ChEA Transcription Factor Binding Site Profiles transcription factor binding site profiles with transcription factor binding evidence at the promoter of MIR4747 gene from the CHEA Transcription Factor Binding Site Profiles dataset.
ChEA Transcription Factor Targets transcription factors binding the promoter of MIR4747 gene in low- or high-throughput transcription factor functional studies from the CHEA Transcription Factor Targets dataset.
ENCODE Histone Modification Site Profiles histone modification site profiles with high histone modification abundance at MIR4747 gene from the ENCODE Histone Modification Site Profiles dataset.
ENCODE Transcription Factor Binding Site Profiles transcription factor binding site profiles with transcription factor binding evidence at the promoter of MIR4747 gene from the ENCODE Transcription Factor Binding Site Profiles dataset.
ENCODE Transcription Factor Targets transcription factors binding the promoter of MIR4747 gene in ChIP-seq datasets from the ENCODE Transcription Factor Targets dataset.
Klijn et al., Nat. Biotechnol., 2015 Cell Line Gene CNV Profiles cell lines with high or low copy number of MIR4747 gene relative to other cell lines from the Klijn et al., Nat. Biotechnol., 2015 Cell Line Gene CNV Profiles dataset.
MotifMap Predicted Transcription Factor Targets transcription factors regulating expression of MIR4747 gene predicted using known transcription factor binding site motifs from the MotifMap Predicted Transcription Factor Targets dataset.
Roadmap Epigenomics Histone Modification Site Profiles histone modification site profiles with high histone modification abundance at MIR4747 gene from the Roadmap Epigenomics Histone Modification Site Profiles dataset.