MIR6511A3 Gene

HGNC Family Non-coding RNAs
Name microRNA 6511a-3
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 set of abstracts provides detailed insights into the regulation of glycogen metabolism, especially under conditions of hypoxia and in the context of glycogen storage diseases. For instance, one study demonstrates that under low‐oxygen conditions, HIF-mediated transcriptional activation of enzymes such as muscle glycogen synthase (GYS1) and other key players leads to marked glycogen accumulation as part of the metabolic adaptation to hypoxia."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " However, none of these findings mention or characterize any function for MIR6511A3.\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAnother set of studies focuses on the pathological consequences of impaired glycogen branching enzyme (GBE1) activity. In a severe model of glycogen storage disease type IV, loss of GBE1 was linked to abnormal cardiac development and early lethality, while in related investigations, even moderate deficiencies in GBE1 altered cellular bioenergetics, redox balance, and mitochondrial respiration."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": " Again, within the context of these studies, MIR6511A3 does not emerge as a mediator or regulator.\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFinally, research examining mild GBE1 reduction in aged tissues highlighted increased oxidative stress and shifts in mitochondrial function, suggesting that subtle changes in glycogen structure can have broader impacts on cellular homeostasis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": " Overall, while these abstracts collectively underscore the complexity of glycogen metabolism and its integration with cellular bioenergetics, they do not report any role or function for MIR6511A3. Consequently, based on the provided literature, the function of MIR6511A3 remains undetermined, and further targeted studies would be needed to explore any potential regulatory interactions between MIR6511A3 and the metabolic pathways highlighted.\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Nuria Pescador, Diego Villar, Daniel Cifuentes, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Hypoxia promotes glycogen accumulation through hypoxia inducible factor (HIF)-mediated induction of glycogen synthase 1."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "PLoS One (2010)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1371/journal.pone.0009644"}], "href": "https://doi.org/10.1371/journal.pone.0009644"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "20300197"}], "href": "https://pubmed.ncbi.nlm.nih.gov/20300197"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Yi-Ching Lee, Chia-Jung Chang, Deeksha Bali, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Glycogen-branching enzyme deficiency leads to abnormal cardiac development: novel insights into glycogen storage disease IV."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Hum Mol Genet (2011)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1093/hmg/ddq492"}], "href": "https://doi.org/10.1093/hmg/ddq492"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "21075835"}], "href": "https://pubmed.ncbi.nlm.nih.gov/21075835"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Dominika Malinska, Giorgia Testoni, Malgorzata Bejtka, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Alteration of mitochondrial function in the livers of mice with glycogen branching enzyme deficiency."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Biochimie (2021)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.biochi.2021.04.001"}], "href": "https://doi.org/10.1016/j.biochi.2021.04.001"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "33857563"}], "href": "https://pubmed.ncbi.nlm.nih.gov/33857563"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Dominika Malinska, Giorgia Testoni, Jordi Duran, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Hallmarks of oxidative stress in the livers of aged mice with mild glycogen branching enzyme deficiency."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Arch Biochem Biophys (2020)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.abb.2020.108626"}], "href": "https://doi.org/10.1016/j.abb.2020.108626"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "33049291"}], "href": "https://pubmed.ncbi.nlm.nih.gov/33049291"}]}]}]}
Synonyms MIR6511A-3, HSA-MIR-6511A-3
NCBI Gene ID 102465683
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Predicted Functions View MIR6511A3's ARCHS4 Predicted Functions.
Co-expressed Genes View MIR6511A3's ARCHS4 Predicted Functions.
Expression in Tissues and Cell Lines View MIR6511A3's ARCHS4 Predicted Functions.

Functional Associations

MIR6511A3 has 0 functional associations with biological entities spanning 0 categories () extracted from 0 datasets.

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Dataset Summary