ArticleThe Journal of biological chemistry2011
Large scale RNAi screen reveals that the inhibitor of DNA binding 2 (ID2) protein is repressed by p53 family member p63 and functions in human keratinocyte differentiation.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- TNF-α-Induced Downregulation of ID2 in Human First Trimester Trophoblast Cells.Asian journal of biological sciences · 2025Article
- Article
- Functional annotation of lncRNA in high-throughput screening.Essays in biochemistry · 2021Review
- A kinome-targeted RNAi-based screen links FGF signaling to H2AX phosphorylation in response to radiation.Cellular and molecular life sciences : CMLS · 2015Article
- p53 and ΔNp63α Coregulate the Transcriptional and Cellular Response to TGFβ and BMP Signals.Molecular cancer research : MCR · 2015Article
- Article
- RNAi screening: new approaches, understandings, and organisms.Wiley interdisciplinary reviews. RNAReview
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inhibitor of DNA binding 2, dominant negative helix-loop-helix protein, ID2, acts as an oncogene and elevated levels of ID2 have been reported in several malignancies. Whereas some inducers of the ID2 gene have been characterized, little is known regarding the proteins capable to repress its expression. We developed siRNA microarrays to perform a large scale loss-of-function screen in human adult keratinocytes engineered to express GFP under the control of the upstream region of ID2 gene. We screened the effect of siRNA-dependent inhibition of 220 cancer-associated genes on the expression of the ID2::GFP reporter construct. Three genes NBN, RAD21, and p63 lead to a repression of ID2 promoter activity. Strikingly NBN and RAD21 are playing on major role in cell cycle progression and mitosis arrest. These results underline the pregnant need to silence ID2 expression at transcript level to promote cell cycle exit. Central to this inhibitory mechanism we find p63, a key transcription factor in epithelial development and differentiation, which binds specific cis-acting sequence within the ID2 gene promoter both in vitro and in vivo. P63 would not suppress ID2 expression, but would rather prevent excessive expression of that protein to enable the onset of keratinocyte differentiation.
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