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Homo sapiens (human) NPPA antisense RNA 1 (NPPA-AS1) URS000075D3D8_9606

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NPPA-AS1: NPPA-AS1 is a natural antisense transcript that has been shown to play a role in various heart disease conditions, including atrial fibrillation (AF) [PMC7432754]. In mouse hearts, inhibition of NPPA-AS1 increased the expression levels of Nppa, suggesting its therapeutic potential [PMC7432754]. NPPA-AS1 negatively regulates NPPA expression by enhancing the binding of the RE1-silencing transcription factor (REST) to the NPPA promoter, resulting in suppression of NPPA gene expression [PMC7432754]. It has been found that NPPA-AS1 is localized to the nucleus in iPSC-CMs [PMC7432754]. Co-expression analysis revealed that NPPA-AS1 is co-expressed with six contractile genes, suggesting its involvement in AF pathogenesis through modulation of cardiac contraction [PMC7432754]. Additionally, it has been predicted that NPPA-AS1 interacts with genes such as ITGB3 and HSF2 and may be involved in AF pathogenesis [PMC7432754]. NPPA-AS1 has also been shown to play a role in cardiac DNA repair and cell cycle re-entry. It competitively binds to the splicing factor SFPQ and displaces NONO from the SFPQ/NONO dimer required for DNA break repair. Deletion of NPPA-AS1 decreased DNA damage and promoted cardiomyocyte cell cycle re-entry, suggesting its potential therapeutic effect against myocardial infarction [PMC9563854]. Furthermore, differential expression of NPPA-AS1 has been observed in various diseases such as esophageal squamous cell carcinoma (ESCC) and heart failure (HF) [PMC5337622] [PMC10070117] [PMC9775550]. In ESCC tissue samples, differential expression of NPPA-AS1 suggests its potential function in ESCC [PMC5337622]. In HF, NPPA-AS1 expression is elevated in the myocardium, making it an interesting target for therapeutic intervention [PMC9775550]. In summary, NPPA-AS1 is a natural antisense transcript that regulates NPPA expression and is involved in various heart disease conditions. Its therapeutic potential has been demonstrated in mouse models and it has been implicated in AF pathogenesis, cardiac DNA repair, and cell cycle re-entry. Its differential expression has also been observed in diseases such as ESCC and HF. Further research is needed to fully understand the therapeutic implications of targeting NPPA-AS1 [PMC7432754] [PMC9563854] [PMC5337622] [PMC10070117] [PMC9775550].

Genome locations

Gene Ontology annotations

Sequence

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AUUCCCAGUCACCCACUCACUCAGAAAGCCGGGAGUCAUCGGACACCUUGCUGGUCAGAGGUCCUGGGGGUGGUUUUGAACCAUCAGAGCUUGGACUUUUCUGACUUCCCCAGCAAGGAUCUUCCCACUUCCUGCUCCCUGUGUUCCCACCCUCCAGUGUUGGCACAGGCCCACCCCUGGCUCCACCAGAGCCAGAAGCAGAGGUAGAAUCAGGCGGGCCCCGGGCUGCACUCCGAGCAGUGUUCCUGGCCAUCUUUGCUACUUUCCUAGAGAACCCGGCUGUUGCCUUAAAUGUGUGAGAGGGACUUGGCCAAGGCAAAAGCUGGGGAGAUGCCAGUGACAACAUACAGUUCAUGACUAGGUUUAGGAAUUGGGCACUGAGAAAAUUCUCAAUAUUUCAGAGAGUCCUUCCCUUAUUUGGGACUCUUAACACGGUAUCCUCGCUAGUUGGUUUUAAGGGAAACACUCUGCUCCUGGGUGUGAGCAGAGGCUCUGGUCUUGCCCUGUGGUUUGACUCUCCUUAGAACCACCGCCCACCAGAAACAUAAAGGAUUAAAAUCACACUAAUAACCCCUGGAUGGUCAAUCUGAUAAUAGGAUCAGAUUUACGUCUACCCUAAUUCUUAACAUUGCAGCUUUCUCUCCAUCUGCAGAUUAUUCCCAGUCUCCCAGUAACACGUUUCUACCCAGAUCCUUUUUCAUUUCCUUAAGUUUUGAUCUCCGUCUUCCUGAUGAAGCAGGCAGAGCUCAGAGGAUCUUGGCAUCACCCACCAAAGUUAGCUGAAAGCAGGGCACUCCUGGAUAAAGCAGCUUCACUCAACUCUGGGGAAUGCUACCAUUUUUUUUCCAAAGUAGAAAGGAAGCACUUCUGAGCCAGUGACCACUGAAAGAUGAACACUCUUCCUGAUCCUCUCCUCUAGAAUUCAUCUCCUCCUGCUAGCAGCCGCGUCCUGGAGGAGCAGCGGAUGGGGAAUCCAUUCUGUUUCUUCCUGGUGUUUAGGAAGUUGCCCCACACACAGAUUGCCCCGAUGUCCAACCAGAAGAAGUGAAACUGCUGCUGGGUCUGGAGAGGUGAAGACCCGUGGCCAGCUUCUGUUGUUGCCAUCGGCCAUUGCUUUUUGUUCGCUUGCUUUUGGUUUUGCAAGAAGAGCGGCCUCUGUCUCUGAUCUGCUUCAAAUCAUCAUUCCAUCAGUGACAGAAGUGGCUGUUCCAUCAGUGGUCGCAGCCAGUUCAGCUCCUGCAUCCAUCCCCAAGUGUUCUGAGUGGAAUUUGAGGCCUCCCCAACCACCUACCAAAAAAGGAGGGUGAAAUGAAAGGAAGAAGAAAAACUCAGCAUUCUUUCCUCUGACAAAGAGUAAAACGACAAGGAAUAUCGGCCUGAAUUCUCUUCCCAAGAAGAAAGAAAGCACACCAACGCAGGCAUUUGUCUUCUGUCCAUGGUGCUGAAGUUUAUUCACUUUCAAACCACUUUCAGUAACAGCAAAUUCUUUAGAAAAGGAAAAUACAGGGAAAGGGAUAAACCUCACUGACUUGGAGGAAAUCAAGAGGAGUGAGCACAGCAUCAGAAAGCCCCCUGGCCCCAGACUGCACCCGCUUUCCUGGCCCUACCUUGAAAUCCAUCAGGUCUGCGUUGGACACGGCAUUGUACAUGGGAUUAGCUCUG

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