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Homo sapiens (human) HDAC4 antisense RNA 1 (HDAC4-AS1) URS00007DB98B_9606

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HDAC4-AS1: HDAC4-AS1 is a long non-coding RNA (lncRNA) that is upregulated in hypoxic conditions and downregulated after reoxygenation [PMC8431062]. It has been shown to bind to the HDAC4 promoter and facilitate the recruitment of hypoxia-inducible factor 1 (HIF-1) [PMC8431062]. HDAC4-AS1 inhibits HDAC4 expression in human ARPE-19 cells exposed to hypoxic stress [PMC8431062]. The transcripts of HDAC4-AS1 can be applied to the basic regulatory model of HDAC4 [PMC8806694]. It has been found that HDAC4-AS1 can bind to the promoter region and suppress HDAC4 transcription in hypoxic ARPE-19 cells [PMC8806694]. The findings suggest that HDAC4-AS1 might be one of the novel candidates responding to oxygen concentration in ARPE-19 cells [PMC8806694]. From an evolutionary perspective, HDAC4-AS1 may have developed from an enhancer element and acts as a unique factor for regulating HDAC4 transcription [PMC8806694]. The expression of HDAC4 is opposite to that of HDAC4-AS1, indicating that HDAC4-AS1 may play a suppressive effect on its transcription [PMC8806694]. HDAC4-AS1 interacts with HIF-α, and HIF-α knockdown weakens its interaction with the promoter region, indicating its crucial role in suppressive regulation of HDAC4-AS1 on HDAC4 transcription under hypoxic stress conditions [PMC8806694]. Knockdown or overexpression experiments have shown that HDAC4-AS1 can regulate HDAC4 transcription activity under hypoxic conditions [PMC8806694]. HDAC4-AS1 is a regulatory target that responds to oxygen concentration in RPE cells and acts as a bridge between HIF-1α and HDAC4 transcriptional activity [PMC8806694].

Genome locations

Gene Ontology annotations

Sequence

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UCGCGGUUGAGGAGGCGCAGGGACCGGGGGCCAGUAGUGGCCGUAAACACGGGCCCCGGCCGUGUCCGGUCGCACUCGGUAGCCCGCAUGGCUGCCUAGCGGAGUAUGACAACUUUUCAACUUGAGUGCACACACUGUCCCCGGAAUCCCGCGUUCCAGGGAGGAAGCGCCUUUGACAGCGCGCGCCGGUUCGUGGGGCCCGACGGCGUGGGCCUGUGGUUGCGGACCUGGCGGAGAUGCGCGUUCGCUUCGAUUGUAGGCCAUUCCUUUUAGGAGCUGAGAAAGGAUCCGUUUUUACAGCAUUCUCGACCUGUGAUUCUUGGUGGGGGAAACUAGUUAUGUGGAUAAAAAUACAGUUAGCAAAAUAAAAAUGCCAAUUUUACA

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Publications