MIR4744 Gene

HGNC Family Non-coding RNAs
Name microRNA 4744
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": "\nSeveral studies have highlighted the importance of proteolytic enzymes in a range of physiological and pathophysiological processes. For instance, neurolysin—a metalloendopeptidase involved in the catabolism of bioactive peptides—has been implicated in modulating angiogenesis, brain responses to ischemic injury, energy metabolism, and even brain morphology. Disruption of neurolysin function alters the balance of vasoactive and neuromodulatory peptides, thereby affecting tumor growth by restricting hypoxic diffusion"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ", modulating the renin-angiotensin system through a novel, high-affinity angiotensin binding site"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": ", and influencing outcomes after ischemic stroke by regulating neuropeptide levels."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": " Moreover, studies in insulin-sensitive pathways indicate that neurolysin loss improves glucose tolerance and insulin signaling"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": ", while further work confirms that enhanced neurolysin expression in the brain protects against ischemic injury"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": "and even affects brain morphology."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn contrast to the regulation imparted by proteolytic enzymes, recent evidence has revealed that microRNA‐4744 (miR‑4744) functions as a key post‐transcriptional regulator in glioma. Specifically, miR‑4744 directly binds to the 3′‑untranslated region of the mRNA encoding the oncogenic factor RIOK2, leading to its down-regulation. This interaction results in reduced expression of RIOK2 and subsequent inhibition of matrix metalloproteinases and mesenchymal markers, thereby impeding glioma cell migration, invasion, and the epithelial–mesenchymal transition. Notably, glioma tissues display lower levels of miR‑4744 alongside elevated RIOK2 expression, underscoring the role of miR‑4744 loss in promoting tumor cell infiltration and suggesting its potential as a therapeutic target."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Thaysa Paschoalin, Adriana K Carmona, Elaine G Rodrigues, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Characterization of thimet oligopeptidase and neurolysin activities in B16F10-Nex2 tumor cells and their involvement in angiogenesis and tumor growth."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Mol Cancer (2007)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1186/1476-4598-6-44"}], "href": "https://doi.org/10.1186/1476-4598-6-44"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "17620116"}], "href": "https://pubmed.ncbi.nlm.nih.gov/17620116"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Naomi J Wangler, Kira L Santos, Ines Schadock, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Identification of membrane-bound variant of metalloendopeptidase neurolysin (EC 3.4.24.16) as the non-angiotensin type 1 (non-AT1), non-AT2 angiotensin binding site."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Biol Chem (2012)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1074/jbc.M111.273052"}], "href": "https://doi.org/10.1074/jbc.M111.273052"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "22039052"}], "href": "https://pubmed.ncbi.nlm.nih.gov/22039052"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Mamoon Rashid, Naomi J Wangler, Li Yang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Functional up-regulation of endopeptidase neurolysin during post-acute and early recovery phases of experimental stroke in mouse brain."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Neurochem (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1111/jnc.12513"}], "href": "https://doi.org/10.1111/jnc.12513"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "24164478"}], "href": "https://pubmed.ncbi.nlm.nih.gov/24164478"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Diogo M L P Cavalcanti, Leandro M Castro, José C Rosa Neto, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Neurolysin knockout mice generation and initial phenotype characterization."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Biol Chem (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1074/jbc.M113.539148"}], "href": "https://doi.org/10.1074/jbc.M113.539148"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "24719317"}], "href": "https://pubmed.ncbi.nlm.nih.gov/24719317"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "Srinidhi Jayaraman, Abdullah Al Shoyaib, Joanna Kocot, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Peptidase neurolysin functions to preserve the brain after ischemic stroke in male mice."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Neurochem (2020)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1111/jnc.14864"}], "href": "https://doi.org/10.1111/jnc.14864"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "31486527"}], "href": "https://pubmed.ncbi.nlm.nih.gov/31486527"}]}, {"type": "r", "ref": 6, "children": [{"type": "t", "text": "Robert C Speth, Eduardo J Carrera, Catalina Bretón, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Distribution of non-AT1, non-AT2 binding of 125I-sarcosine1, isoleucine8 angiotensin II in neurolysin knockout mouse brains."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "PLoS One (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1371/journal.pone.0105762"}], "href": "https://doi.org/10.1371/journal.pone.0105762"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "25147932"}], "href": "https://pubmed.ncbi.nlm.nih.gov/25147932"}]}, {"type": "r", "ref": 7, "children": [{"type": "t", "text": "Yunnong Song, Cheng Li, Lei Jin, et al. "}, {"type": "b", "children": [{"type": "t", "text": "RIOK2 is negatively regulated by miR-4744 and promotes glioma cell migration/invasion through epithelial-mesenchymal transition."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Cell Mol Med (2020)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1111/jcmm.15107"}], "href": "https://doi.org/10.1111/jcmm.15107"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "32125767"}], "href": "https://pubmed.ncbi.nlm.nih.gov/32125767"}]}]}]}
NCBI Gene ID 100616420
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Download Associations
Predicted Functions View MIR4744's ARCHS4 Predicted Functions.
Co-expressed Genes View MIR4744's ARCHS4 Predicted Functions.
Expression in Tissues and Cell Lines View MIR4744's ARCHS4 Predicted Functions.

Functional Associations

MIR4744 has 281 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 MIR4744 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 MIR4744 gene relative to other cell lines from the CCLE Cell Line Gene CNV Profiles dataset.
COSMIC Cell Line Gene CNV Profiles cell lines with high or low copy number of MIR4744 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 MIR4744 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 MIR4744 gene from the ENCODE Transcription Factor Binding Site Profiles dataset.
ENCODE Transcription Factor Targets transcription factors binding the promoter of MIR4744 gene in ChIP-seq datasets from the ENCODE Transcription Factor Targets dataset.
GTEx Tissue Gene Expression Profiles tissues with high or low expression of MIR4744 gene relative to other tissues from the GTEx Tissue Gene Expression Profiles dataset.
Klijn et al., Nat. Biotechnol., 2015 Cell Line Gene CNV Profiles cell lines with high or low copy number of MIR4744 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 MIR4744 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 MIR4744 gene from the Roadmap Epigenomics Histone Modification Site Profiles dataset.