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Damage induced long noncoding RNA (DINO) is a conserved, noncoding RNA transcribed in response to cellular DNA damage, most strongly induced by agents such as doxorubicin, and regulated by p53. As a lncRNA, DINO does not encode a protein but instead binds physically to p53, promoting its stability, amplifying its signaling, and ensuring robust transcriptional activation of p53-dependent genes involved in cell cycle arrest and apoptosis. DINO provides an auto-amplification loop within the p53 network: DNA damage induces DINO, which in turn stabilizes and activates p53, further driving expression of stress response genes. Loss or silencing of DINO blunts p53 signaling, reduces cell cycle arrest and apoptosis in response to DNA damage, and in experimental models, protects against excessive p53-driven cell death such as in acute radiation syndrome. While DINO is not currently a direct drug target, it plays a crucial role in the integrity of the DNA damage response pathway and may influence the efficacy of p53-targeted cancer therapies
Not applicable; DINO function is indirect modulation of p53, not a conventional drug target. Drugs acting on p53 may be indirectly affected by DINO status, but DINO is not directly targeted
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