| HGNC Family | Non-coding RNAs |
| Name | microRNA 3942 |
| 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 collection of studies provided offers an extensive overview of the multifaceted roles of T-type calcium channels—especially the CaV3.2 isoform—in regulating vascular tone, cardiac and neuronal excitability, nociceptive signaling, synaptic transmission, development, and other physiological processes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFurther work in this set of abstracts addresses mechanisms by which CaV3.2 channels influence pain processing, epileptogenesis, synaptic transmission and intracellular signaling in diverse cell types and tissues. These include modulation through redox regulation, deubiquitination by USP5, interactions with TRP channels, regulation by auxiliary subunits, and activity‐dependent plasticity—all of which underscore the channels’ central roles in cellular excitability and signaling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional investigations extend the impact of CaV3.2 channel modulation to learning and memory, osteocyte mechanosensation, embryonic development, sperm physiology, gastrointestinal motility, and renal hemodynamics. These studies reveal how changes in CaV3.2 expression and activity—whether through interactions with environmental factors (such as hydrogen sulfide, nitrous oxide, or cannabinoids) or through alterations in intracellular signaling cascades—influence a broad spectrum of biological functions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMeanwhile, several studies have focused on the molecular and cellular regulation of CaV3.2 channels—exploring roles for deubiquitinases like USP5, interactions with actin-binding proteins such as Kelch-like 1, and the consequent effects on neuron excitability, pain hypersensitivity, and neurodegenerative conditions—further illustrating the channels’ clinical relevance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "34", "end_ref": "42"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFurthermore, pharmacological modulation of CaV3.2 channels and their contributions to analgesia, anti-hyperalgesia, neuroprotection, and even chemotherapeutic cardiotoxicity have been examined, emphasizing their diverse roles in both normal physiology and disease states."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "43", "end_ref": "46"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nLastly, complementary studies have addressed how CaV3.2 channels influence vascular biomechanics, neuronal progenitor behavior, and sensory neuron development—in turn modulating arterial tone and renal function—thereby highlighting the comprehensive impact of these channels across multiple organ systems."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "47", "end_ref": "50"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nNotably, despite the extensive insights into T-type calcium channel biology provided by these publications, none of the studies explicitly mention or investigate MIR3942. 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"}, {"type": "b", "children": [{"type": "t", "text": "Differential effect of T-type voltage-gated Ca2+ channel disruption on renal plasma flow and glomerular filtration rate in vivo."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Am J Physiol Renal Physiol (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1152/ajprenal.00016.2014"}], "href": "https://doi.org/10.1152/ajprenal.00016.2014"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "24966091"}], "href": "https://pubmed.ncbi.nlm.nih.gov/24966091"}]}]}]}
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| NCBI Gene ID | 100500904 |
| API | |
| Download Associations | |
| Predicted Functions |
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| Co-expressed Genes |
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| Expression in Tissues and Cell Lines |
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MIR3942 has 204 functional associations with biological entities spanning 3 categories (molecular profile, cell line, cell type or tissue, gene, protein or microRNA) extracted from 10 datasets.
Click the + buttons to view associations for MIR3942 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 MIR3942 gene relative to other cell lines from the CCLE Cell Line Gene CNV Profiles dataset. | |
| ENCODE Histone Modification Site Profiles | histone modification site profiles with high histone modification abundance at MIR3942 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 MIR3942 gene from the ENCODE Transcription Factor Binding Site Profiles dataset. | |
| ENCODE Transcription Factor Targets | transcription factors binding the promoter of MIR3942 gene in ChIP-seq datasets from the ENCODE Transcription Factor Targets dataset. | |
| GTEx Tissue Gene Expression Profiles | tissues with high or low expression of MIR3942 gene relative to other tissues from the GTEx Tissue Gene Expression Profiles dataset. | |
| JASPAR Predicted Transcription Factor Targets | transcription factors regulating expression of MIR3942 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 MIR3942 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 MIR3942 gene from the KnockTF Gene Expression Profiles with Transcription Factor Perturbations dataset. | |
| MotifMap Predicted Transcription Factor Targets | transcription factors regulating expression of MIR3942 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 MIR3942 gene from the Roadmap Epigenomics Histone Modification Site Profiles dataset. | |