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Homo sapiens (human) antisense of IGF2R non-protein coding RNA (AIRN) URS000041E62F_9606

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AIRN: AIRN, an imprinted long non-coding RNA (lncRNA), has been shown to play a role in various biological processes [PMC9520944]. Overexpression of AIRN in liver sinusoidal endothelial cells (LSEC) was found to increase the protein levels of VEGFR2, eNOS, and VE-Cadherin, which are important for LSEC function [PMC9520944]. The interaction between AIRN and IMP2 was elucidated for the first time in a study, revealing that AIRN influences the stability of IMP2 [PMC9670606]. Furthermore, AIRN was found to be beneficial for liver fibrosis by maintaining LSEC differentiation and may serve as a serum biomarker for liver fibrogenesis [PMC9520944]. In a liver fibrosis model, AIRN was found to be overexpressed [PMC9520944]. Overexpression of AIRN also mitigated hepatocyte apoptosis induced by H2O2 [PMC9828194]. The DNA methylation of the ectopic AIRN ICR remained high even after cultivation of mouse embryonic stem cells in 2i medium for 10 days [PMC9649441]. The expression of a truncated AIRN transcript was preserved while transcription across the Igf2r promoter was abolished [PMC4819931]. The interaction between AIRN and Slc22a3 promoter was shown to place these loci in close proximity in the nuclear space but is not essential for upregulating Slc22a3 expression on the maternal allele [PMC6675118]. Histone methylation patterns are critical for parent-specific expression of Igf2r and AIRN genes [PMC3335465]. It has been proposed that AIRN recruits histone modifying complexes EHMT2, PRC1, and PRC2 to distant imprinted genes in extra-embryonic tissues [PMC6675118].

Genome locations

Gene Ontology annotations

Sequence

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GAAAGCACACACCAUGCUGGAAAGGAGAGAGAAGGAAAAACCCACUCCUAGCCACACAAUGGUGGAUCUUAAUAUCCAAUGAAAAGAAAAAAUUCUAAUCUAGGUCACACACAAUAACCCAAUAUAAAAUGAACAAGACAUGAUCAAGCAAAUCAAAGAAAAAUGUACAUCAAUAAAUAUGUUAAGACAUGUUCAAUGUUACUGGUGAUCAAGGAAUUUCAAAUCAAGACCAAAAUGGUAUACCAUUUACAACCAUCCCUCUGGCAAAAAUUAAAUACCAAGUGUCAGCCAUGAGGUGGCUCAGAGCUCUCCUGUAUUGCUAGUGAAAUGUUAACUGGUUCAACAACUAUGUAAGUCAGCAGGACAUUAUGUCCUAAAAUUGAACAUUCGUGUGCCCUAUGACCUAGUUACUCCACUCAGGUCUAUAUAAAAGAGAAAACCAUGCACAUAUGGAACAUGCACAGCAGAAAAUGUGAAAGAAUAUCUCAUGCUCUUCAGAAGAGCAAAAACCUGGAAAUGACCAAAGGCCCAUCAACAGAAGAGUGGAUAAAUUAACUUCAGCAGAUCCACACAAAAUAUCACAGCAGUCAGAAGGAAUAAACCACAGUGAAAAACAACAAUACGGUUGAUUUUUAGUAAUAUUACUGUUAUCACUUAAGUCCCAAAAAGUUACACAUAGGAAGAUAACUUAGUUGCAAACACACAGAUUUUUUUUUUUUGGAAAUUAGAUACAGUAAAAAAAAAAAAAAAUUAAUACAAGAUGGGAGCUAAUGAUUACUCCUAGCGAAAAGUGAAAGAGGAAAGAGUAAAACAGAUAGUGGUUACUGCCAAGAUCCUAGAUUUUUGUUGGAAACAGUGCUCGCUACAUUAUACAAAACAACUAAUUUUUUAAAAGGAAAAAGGUUAGUCUAUGGAUUAACACAUGGCUCACUGUACGUGCCAUGAGCUCGGGAUGAUAGCUGAUCCAAUCCCAUAUACACCUGAAGUCUUGGGGCAGGGGCGGACCACGAGUCAGCGCGCCCCCACAGCACCAGGCUGAUGGCCCCGUGGUUCUUCUGCCUGCAAGCAAAAGUCAGCCACGAUCAUCCUUCUCCAUCUGCAACACCCAGGGUCUUUUCUAAAACUUUUGCCCAGUCGGCUCAGCCAAAAGGACACAGAAGCCCUGCAGAGGCUCUGAAACCAAGCUGCCAUGGCUCCCAGUUCGACAUCAUGUCACCGGAGCCUGCACAGAUGAACCAAGCUUGCAACACGGGAGGAACCUAAGCGCUGGACUGAGGAGCGGGACUGAAAUAAGAAGCGCACACCACAUGGCAAGAUCCAGGAUCCAAUCAGAUAGAGCCCUGGUGUCAUCUAAUUGCAAGAUCCAAUCAGAACACACCUCAUUACCUUAUGGUAUUGCCAGACUAUCAGGAGAGACCAUAAAUCAGAUAAAAACAUGAGUUGUAUCCAAAACUCAACCAGGUAUCAUCUUAAAUAUCCAACAGAAUUC

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Publications