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Homo sapiens (human) damage induced long noncoding RNA (DINOL) URS0000576071_9606

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DINOL: DINOL, also known as damage-induced noncoding RNA (DINO), is a long noncoding RNA (lncRNA) that has been identified as a p53 binding partner [PMC9697900]. It is involved in amplifying p53-mediated DNA damage response (DDR) signaling [PMC9213768]. DINOL, along with other lncRNAs such as PINCR and NEAT1, is regulated by p53 and induced by DNA damage [PMC9861885]. These lncRNAs are upregulated upon the deletion of Tks4, a gene involved in DNA damage response [PMC9861885]. DINOL has the ability to bind and stabilize p53, contributing to the amplification of TP53-mediated signaling [PMC7238103]. It also plays a role in controlling the expression of genes involved in cell cycle arrest and apoptosis [PMC9861885]. DINOL has been found to have target sites within regions of antisense transcription in the promoters of specific genes [PMC10003719]. Although there have been attempts to reconstruct the Dynamic Interaction Network of Life (DINOL), evolutionary biologists have not yet achieved this goal [PMC5972403]. Furthermore, studies have shown that levels of DINOL increase under nitrogen deficiency conditions in lettuce leaves, along with other compounds such as p-hydroxybenzoic acid, inositol, and stachyose [PMC9968814]. In summary, DINOL is an lncRNA that interacts with p53 and plays a role in amplifying TP53-mediated signaling. It is upregulated upon DNA damage and has target sites within gene promoters. However, reconstructing the Dynamic Interaction Network of Life (DINOL) remains an ongoing challenge for evolutionary biologists.

Genome locations

Gene Ontology annotations

Sequence

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GCCGAGUUCCAGCAGGCCAGCCGGUCCCGGAACCUCGCGUGCUGCAGGAGGGCACUUCCCUCCUCCCCCAGUCCCUCGCCUGCGUUGGUGCGCUGGACACAUUUCCCCACGAAGUGAGCCACAAAUCUGGCUUUUUUUACUUGGAGAAUGAGUUGGCACUCUCCAGGAGGACACAGCACUGUUAGAAUGAGCCCCCUUUCUGGCUCACCGCUGACCCACUCUGGCAGGCAAGGAUUUACCCAAUGCAGCUGAAAAGAUCAGGAGGAUGACAUUAAUACAUAAAAAUUCAUAAAUUAUAAAAACGAUGCACCUCUCUGCAAUUUCCAGAAAAGCCCCACAAUAUCACCUCUAUUCCCACUGAUCCCUCACUAGGUCACCUCUCCCAGAAGCACCUGGAGCACCUAGACACCCCAACAAAGCAUCUUGAGGCCAGAAUGAUUUUUCAGUCCCGUUUAUUUCACAGAUGAGGAAAUUGAGGUCCACUGAACUUAAGUAUACAAAGUUGUUGAUUGUCACAUGCUUCCGGGAAGGAGGGAAUUGGAGAGACUACCAAAAAAGGGCAACCUGAUCUCCAGGGAAACAGAAGAAUUGGACAUUGAACCAAUCUCCCUACACCCUACACUCACCUGAACAGAAGAAAUCCCUGUGGUUGCAGCAGCUUUGUUGGCCAGGAAGGGGAGGAUUUGACGAGUGAGUUGUCUGUCUCCUGAAUACUCCCCACAUAGCCCGUAUACACUGCUGGGGAAACUGGGGCUCAGAGAAGUCUGGUGACCUAACUCAGAUCAUGCAGCAAAGAAAUGACUAUAGUUGGAACACAGGACUUUUGCCUCCUGCCCGGGGCUCUCUGCUUGUCAUCCUUUAUUUCUGUGGCUCCAAAAUGACAAAAAUGCCAAAUAACCCUCAUUUGCAGAUGGUUUAUGGAGAUGACAUAAAUAAAGGACAAUUCUGGAA

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Publications