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Homo sapiens (human) HIF1A antisense RNA 3 (HIF1A-AS3) URS0000600EEF_9606

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HIF1A-AS3: HIF1A-AS3 is a long non-coding RNA (lncRNA) that is induced and stabilizes HIF1A binding in hypoxia response elements (HRE) in cancer cells [PMC9845402]. It assembles the HIF1A transactivation complex and enhances the expression of HIF1α target genes [PMC9845402]. HIF1A-AS3, along with HIF1A and HIF1A-AS1, is upregulated in Li-infected macrophages [PMC9845402]. It is also identified as one of the 16 prognostic cuproptosis-related lncRNAs, which are associated with cuproptosis-related diseases [PMC9434888]. In a study of hypoxia-related genes, HIF1A-AS3 was found to be upregulated along with other known hypoxia-related genes [PMC7083003]. It was also suggested that HIF1A-AS3 may act as an upstream regulator of hypoxia responses in progressive multiple sclerosis patients [PMC7083003]. Additionally, the involvement of HIF1A-AS3 in neurological diseases was demonstrated, highlighting its potential role in neuroprotection [PMC7083003]. Furthermore, it was found that lncRNA HIF1A-AS3 affects the expression of DNMT3a through downregulation of miR-129-5p [PMC8789170]. References: [PMC9845402] - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9845402/ [PMC9434888] - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9434888/ [PMC7083003] - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7083003/ [PM8789170] - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8789170/

Targeting miRNAs 2 total

According to LncBase, this RNA is targeted by the following miRNAs:

Genome locations

Gene Ontology annotations

Sequence

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UCAUGUAGCGCCAGCCACACCAGGAACAGAAGGGUGCCGGGUACCUUCCGCAUGCUUGGUAUUCUCCCCGCGGGGCUCUGACCGCUGCCGCUCUCAGGCACCUGUCUUUCCUCUCCGUCCCAGAAUGGAGCCAAGACAAGGGAAUAAACGAAAUUCAAUAGUACACGGAGAUCGGGUGUCUGGGCAGCGUCUUGGAAAAACUAUCCACUACAGUACAGGUCAAGUGAAGUUCUUCUGCUGAUAUGUUCUGCUACUGCAUAAGAGACGGAAUCUAUGUUGCCUCGACUGGUCCUGAACUCCUGGGCUAAAGCGAUCCUUCUGCCUUGGCCUCCCAAAGUGCGAGGAUUAUAGGUGUGAGCCACCCAACCUGGCCUUUGCCAGUAUUUUUAAAUCCAAACACCUAUGCAUGGUGCUUACUAAUAACACAGUGGUAUUCUAAACAUUUUUCACCUAUUAUUUAAUCUUUAUUAUUAUCACCAUGUUACAGAUAAGGACCCUGGCUAAAUAGCUUACCCAACAUUACUCCGUUAAUA

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Publications