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Bidirectional transcript from the CDKN1A promoter.
1.5kb single exon.
Sequence runs antisense through a processed LAP3 pseudogene and contains a SINE.
P53 effector gene, acts in response to DNA damage to limit apoptosis while CDKN1A induces cell cycle arrest.
Loss of PANDA leads to the apoptosis of doxorubicin treated cells.
Loss of PANDA affected the expression of many genes during the DNA damage response. Upregulated genes were enriched for those involved in apoptosis, including the apoptotic activators APAF1, BIK, FAS and LRDD. Leading to apoptosis of doxorubicin treated cells.
Cell death genes downstream of p53 are known to have NF-YA binding sites. PANDA RNA interacts with the transcription factor NF-YA and attenuates its occupany of target gene promoters.
One of five lncRNAs surrounding the transcription start site of the cell cycle gene CDKN1A that, along with the CDKN1A protein coding gene, were induced in human fetal lung fibroblasts upon DNA damage by doxorubicin.
Induced up to 40 fold upon DNA damage peaking 16 h after doxorubicin treatment, a much greater response than shown by CDKN1A.
Expression of PANDA and CDKN1A were positively regulated by p53. CDKN1A did not induce PANDA.
Syntenic sequence appear to be present in apes and old world monkeys (the Catarrhini).
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Allelic Information and Variation
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Labs working on this lncRNA
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