ArticleOncogene2002
Inhibition of crystallin expression and induction of apoptosis by lens-specific E1A expression in transgenic mice.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Therapeutic potential of a dual mTORC1/2 inhibitor for the prevention of posterior capsule opacification: An in vitro study.International journal of molecular medicine · 2018Article
- Histone posttranslational modifications and cell fate determination: lens induction requires the lysine acetyltransferases CBP and p300.Nucleic acids research · 2013Article
- Lens fiber cell differentiation and denucleation are disrupted through expression of the N-terminal nuclear receptor box of NCOA6 and result in p53-dependent and p53-independent apoptosis.Molecular biology of the cell · 2010Article
- Retinoic acid signaling in mammalian eye development.Experimental eye research · 2009Review
- HIF-1: an age-dependent regulator of lens cell proliferation.Investigative ophthalmology & visual science · 2008Article
- Overexpression of E2F5/p130, but not E2F5 alone, can inhibit E2F-induced cell cycle entry in transgenic mice.Molecular vision · 2008Article
- Conditional deletion of beta1-integrin from the developing lens leads to loss of the lens epithelial phenotype.Developmental biology · 2007Article
- Distinct embryonic expression and localization of CBP and p300 histone acetyltransferases at the mouse alphaA-crystallin locus in lens.Journal of molecular biology · 2007Article
- Lens cell targetting for gene therapy of prevention of posterior capsule opacification.Gene therapy · 2006Article
- Reversible inactivation of the transcriptional function of P53 protein by farnesylation.BMC biotechnology · 2006Article
- Prevention of posterior capsule opacification by the induction of therapeutic apoptosis of residual lens cells.Gene therapy · 2006Article
- Identification of global gene expression differences between human lens epithelial and cortical fiber cells reveals specific genes and their associated pathways important for specialized lens cell functions.Molecular vision · 2005Article
- Regulation of gene expression by Pax6 in ocular cells: a case of tissue-preferred expression of crystallins in lens.The International journal of developmental biology · 2004Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Previous studies have shown that the adenovirus E1A oncoprotein can bind to and inactivate the retinoblastoma tumor suppressor protein (pRb) and the transcriptional coactivators CBP/p300. In this study, wild-type E1A12S or two deletion mutants (delN, which binds pRb but not CBP/p300; delCR2, which binds to CBP/p300 but not pRb) were linked to the lens-specific alphaA-crystallin promoter, and used to generate transgenic mice. Lens fiber cells expressing E1A12S or delCR2, both of which bind to CBP/p300, failed to upregulate beta-crystallin and gamma-crystallin expression. In contrast, lens fiber cells expressing delN showed significant expression of beta- and gamma-crystallins. Lens fiber cells expressing delN showed cell cycle entry, marked apoptosis, and evidence for p53 activation, while cells expressing either 12S or delCR2 showed limited apoptosis and no evidence for upregulation of the p53-inducible gene p21. Our results suggest that the transcriptional coactivators CBP and/or p300 are required for the dramatic increases in crystallin expression that accompany terminal differentiation in the lens, and also for activation of p53 in response to inactivation of pRb in the lens.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.