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PANDAR:promoter of CDKN1A antisense DNA damage activated RNA
The PANDAR was located approximately 5 kilobases upstream of the CDKN1A transcription start site and was induced upon DNA damage. 
Sequence runs antisense through a processed LAP3 pseudogene and contains a SINE.
PANDA interacts with the transcription factor NF-YA to limit expression of pro-apoptotic genes; PANDA depletion markedly sensitized human fibroblasts to apoptosis by doxorubicin.
DNA damage activates p53-mediated transcription at CDKN1A and PANDA that functions synergistically to mediate cell cycle arrest and survival.
PANDAR could function as a tumor-promoting gene in breast cancer by regulating G1/S transition. 
PANDA interacts with the transcription factor NF-YA to limit expression of pro-apoptotic genes; PANDA depletion markedly sensitized human fibroblasts to apoptosis by doxorubicin. 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.
Expression of PANDA and CDKN1A were positively regulated by p53.
Expression of neither CDKN1A itself nor TP53 was affected by PANDA depletion, suggesting that PANDA is a P53 effector that acts independently of p21-CDKN1A.
PANDAR is up-regulated in breast cancer clinical samples as well as cell lines.
PANDAR enhanced the binding of Bim1 complex to p16INK4A promoter and suppressed p16INK4A expression.
|Primers used in RACE|| 5'-CAGAACTTGGCATGATGGAG-3'
|RT-PCR primers for PANDAR||5'-TGCACACATTTAACCCGAAG-3'||5'-CCCCAAAGCTACATCTATGACA-3'|
|siRNAs for PANDAR||5'-AAUGUGUGCACGUAACAGAUU-3'||5'-GAGAUUUGCAGCAGACACAUU-3'|
- breast cancer 
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During DNA damage, PANDAR is induced by p53. 
Allelic Information and Variation
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Labs working on this lncRNA
- Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California, USA.
- Nanchang Key Laboratory of Cancer Pathogenesis and Translational Research, Center Laboratory, the Third Affiliated Hospital, Nanchang University, Nanchang, P.R. China.
- Hung T, Wang Y, Lin MF, Koegel AK, Kotake Y, Grant GD, et al. Extensive and coordinated transcription of noncoding RNAs within cell-cycle promoters[J]. Nature genetics. 2011,43(7):621-9.
- Sang Y, Tang J, Li S, Li L, Tang X, Cheng C, et al. LncRNA PANDAR regulates the G1/S transition of breast cancer cells by suppressing p16(INK4A) expression[J]. Scientific reports. 2016,6:22366.