| HGNC Family | Non-coding RNAs |
| Name | microRNA 3944 |
| 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 none of the provided abstracts explicitly mention MIR3944, emerging evidence from studies of the E3‐ubiquitin ligase COP1 suggests that microRNAs such as MIR3944 may play roles in fine‐tuning similar regulatory networks. In several reports, COP1 is shown to coordinate the degradation of key metabolic enzymes and transcription factors to maintain energy homeostasis. For example, COP1 collaborates with fasting‐induced modulators to trigger degradation of acetyl‐coenzyme A carboxylase (ACC) in adipose tissue, controls fatty acid synthase levels via adaptor proteins in liver, and influences insulin secretion in pancreatic β cells as well as basal and insulin‐stimulated glucose uptake in brown adipocytes. These findings imply that factors regulating post‐transcriptional events—including candidate microRNAs—could intersect with COP1’s ubiquitination pathway to modulate systemic metabolic responses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn cancer and tumorigenesis, COP1 exerts tumor‐suppressive functions by regulating the stability of oncogenic and tumor‐suppressor proteins. Studies demonstrate that COP1 ubiquitinates and promotes degradation of ETS transcription factors (ETV1, ETV4, and ETV5) in prostate cancer, downregulates the oncoprotein c‑Jun in vivo, and modulates proteins such as MTA1 and C/EBPα to control cell proliferation and differentiation. Moreover, in triple‐negative breast cancer, deletion of COP1 in tumor cells attenuates macrophage chemoattractant secretion through stabilization of key transcriptional regulators. These diverse functions suggest that post‐transcriptional regulators like MIR3944 might similarly impact oncogenic pathways by targeting either COP1 directly or its downstream effectors, warranting further investigation into its potential role in cancer."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "11"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional studies extend the impact of COP1 to developmental and stress‐response contexts. Prenatal inactivation of COP1 in the lung epithelium disrupts branch morphogenesis via the accumulation of ETS transcription factors, while mammalian cryptochromes—core elements of the circadian clock—negatively regulate COP1 activity to control glucocorticoid receptor signaling. Moreover, emerging data point to potential involvement of COP1 in cerebral ischemia‐reperfusion injury, and candidate gene studies in acute lung injury hint at broader roles in tissue responses to stress. Given the pervasive influence of COP1 on protein stability across these systems, it is plausible that MIR3944, like other microRNAs, could modulate developmental or injury response pathways through subtle interactions with the COP1‐mediated ubiquitin–proteasome network."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "15"}]}, {"type": "t", "text": ""}]}]}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ling Qi, Jose E Heredia, Judith Y Altarejos, et al. "}, {"type": "b", "children": [{"type": "t", "text": "TRB3 links the E3 ubiquitin ligase COP1 to lipid metabolism."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Science (2006)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1126/science.1123374"}], "href": "https://doi.org/10.1126/science.1123374"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "16794074"}], "href": "https://pubmed.ncbi.nlm.nih.gov/16794074"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Jianxiu Yu, Rong Deng, Helen H Zhu, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Modulation of fatty acid synthase degradation by concerted action of p38 MAP kinase, E3 ligase COP1, and SH2-tyrosine phosphatase Shp2."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Biol Chem (2013)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1074/jbc.M112.397885"}], "href": "https://doi.org/10.1074/jbc.M112.397885"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "23269672"}], "href": "https://pubmed.ncbi.nlm.nih.gov/23269672"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Wenying Ren, Yingmin Sun, Sarwat Cheema, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Interaction of constitutive photomorphogenesis 1 protein with protein-tyrosine phosphatase 1B suppresses protein-tyrosine phosphatase 1B activity and enhances insulin signaling."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Biol Chem (2013)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1074/jbc.M112.369371"}], "href": "https://doi.org/10.1074/jbc.M112.369371"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "23439647"}], "href": "https://pubmed.ncbi.nlm.nih.gov/23439647"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Rowena Suriben, Kelly A Kaihara, Magdalena Paolino, et al. "}, {"type": "b", "children": [{"type": "t", "text": "β-Cell Insulin Secretion Requires the Ubiquitin Ligase COP1."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cell (2015)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.cell.2015.10.076"}], "href": "https://doi.org/10.1016/j.cell.2015.10.076"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "26627735"}], "href": "https://pubmed.ncbi.nlm.nih.gov/26627735"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "Xingxing Ren, Ningxin Chen, Yawen Chen, et al. "}, {"type": "b", "children": [{"type": "t", "text": "TRB3 stimulates SIRT1 degradation and induces insulin resistance by lipotoxicity via COP1."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Exp Cell Res (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.yexcr.2019.05.009"}], "href": "https://doi.org/10.1016/j.yexcr.2019.05.009"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "31125554"}], "href": "https://pubmed.ncbi.nlm.nih.gov/31125554"}]}, {"type": "r", "ref": 6, "children": [{"type": "t", "text": "Matthew D Lynes, Qian Huang, Carolina Cora, et al. "}, {"type": "b", "children": [{"type": "t", "text": "A CRISPR Screen Identifies the E3 Ubiquitin Ligase Rfwd2 as a Negative Regulator of Glucose Uptake in Brown Adipocytes."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Genes (Basel) (2023)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.3390/genes14101865"}], "href": "https://doi.org/10.3390/genes14101865"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "37895214"}], "href": "https://pubmed.ncbi.nlm.nih.gov/37895214"}]}, {"type": "r", "ref": 7, "children": [{"type": "t", "text": "Da-Qiang Li, Kazufumi Ohshiro, Sirigiri Divijendra Natha Reddy, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "Cop1 constitutively regulates c-Jun protein stability and functions as a tumor suppressor in mice."}]}, {"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/JCI45784"}], "href": "https://doi.org/10.1172/JCI45784"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "21403399"}], "href": "https://pubmed.ncbi.nlm.nih.gov/21403399"}]}, {"type": "r", "ref": 9, "children": [{"type": "t", "text": "Alberto C Vitari, Kevin G Leong, Kim Newton, et al. 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| NCBI Gene ID | 100500911 |
| 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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MIR3944 has 753 functional associations with biological entities spanning 3 categories (molecular profile, cell line, cell type or tissue, gene, protein or microRNA) extracted from 13 datasets.
Click the + buttons to view associations for MIR3944 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 MIR3944 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 MIR3944 gene from the CHEA Transcription Factor Binding Site Profiles dataset. | |
| ChEA Transcription Factor Targets | transcription factors binding the promoter of MIR3944 gene in low- or high-throughput transcription factor functional studies from the CHEA Transcription Factor Targets dataset. | |
| COSMIC Cell Line Gene CNV Profiles | cell lines with high or low copy number of MIR3944 gene relative to other cell lines from the COSMIC Cell Line Gene CNV Profiles dataset. | |
| ENCODE Histone Modification Site Profiles | histone modification site profiles with high histone modification abundance at MIR3944 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 MIR3944 gene from the ENCODE Transcription Factor Binding Site Profiles dataset. | |
| ENCODE Transcription Factor Targets | transcription factors binding the promoter of MIR3944 gene in ChIP-seq datasets from the ENCODE Transcription Factor Targets dataset. | |
| GTEx Tissue Gene Expression Profiles | tissues with high or low expression of MIR3944 gene relative to other tissues from the GTEx Tissue Gene Expression Profiles dataset. | |
| JASPAR Predicted Transcription Factor Targets | transcription factors regulating expression of MIR3944 gene predicted using known transcription factor binding site motifs from the JASPAR Predicted Transcription Factor Targets dataset. | |
| Klijn et al., Nat. Biotechnol., 2015 Cell Line Gene CNV Profiles | cell lines with high or low copy number of MIR3944 gene relative to other cell lines from the Klijn et al., Nat. Biotechnol., 2015 Cell Line Gene CNV Profiles dataset. | |
| KnockTF Gene Expression Profiles with Transcription Factor Perturbations | transcription factor perturbations changing expression of MIR3944 gene from the KnockTF Gene Expression Profiles with Transcription Factor Perturbations dataset. | |
| MotifMap Predicted Transcription Factor Targets | transcription factors regulating expression of MIR3944 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 MIR3944 gene from the Roadmap Epigenomics Histone Modification Site Profiles dataset. | |