ArticleMolecular and cellular biology2012
p19Arf represses platelet-derived growth factor receptor β by transcriptional and posttranscriptional mechanisms.
Article in Molecular and cellular biology, 2012. 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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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- Methyltransferase Inhibition Enables TgfMolecular and cellular biology · 2023Article
- The Senescence Markers p16INK4A, p14ARF/p19ARF, and p21 in Organ Development and Homeostasis.Cells · 2022Review
- NovelCold Spring Harbor molecular case studies · 2019Article
- Small mitochondrial Arf (smArf) protein corrects p53-independent developmental defects ofProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Tumor suppressor ARF regulates tissue microenvironment and tumor growth through modulation of macrophage polarization.Oncotarget · 2016Article
- p19(Arf) limits primary vitreous cell proliferation driven by PDGF-B.Experimental eye research · 2016Article
- Negative regulation of initial steps in skeletal myogenesis by mTOR and other kinases.Scientific reports · 2016Article
- Isolation and characterization of mammalian cells expressing the Arf promoter during eye development.BioTechniques · 2014Article
- RIG-I-like receptor LGP2 protects tumor cells from ionizing radiation.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- ARF sees Pdgfrβ through the miR.Cell cycle (Georgetown, Tex.) · 2014Article
- miR-34a is essential for p19(Arf)-driven cell cycle arrest.Cell cycle (Georgetown, Tex.) · 2014Article
- A distant, cis-acting enhancer drives induction of Arf by Tgfβ in the developing eye.Developmental biology · 2013Article
- Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
In addition to cancer surveillance, p19(Arf) plays an essential role in blocking signals stemming from platelet-derived growth factor receptor β (Pdgfrβ) during eye development, but the underlying mechanisms have not been clear. We now show that without Arf, pericyte hyperplasia in the eye results from enhanced Pdgfrβ-dependent proliferation from embryonic day 13.5 (E13.5) of mouse development. Loss of Arf in the eye increases Pdgfrβ expression. In cultured fibroblasts and pericyte-like cells, ectopic p19(Arf) represses and Arf knockdown enhances the expression of Pdgfrβ mRNA and protein. Ectopic Arf also represses primary Pdgfrβ transcripts and a plasmid driven by a minimal promoter, including one missing the CCAAT element required for high-level expression. p19(Arf) uses both p53-dependent and -independent mechanisms to control Pdgfrβ. In vivo, without p53, Pdgfrβ mRNA is elevated and eye development abnormalities resemble the Arf (-/-) phenotype. However, effects of p53 on Pdgfrβ mRNA do not appear to be due to direct p53 or RNA polymerase II recruitment to the promoter. Although p19(Arf) controls Pdgfrβ mRNA in a p53-dependent manner, it also blunts Pdgfrβ protein expression by blocking new protein synthesis in the absence of p53. Thus, our findings demonstrate a novel capacity for p19(Arf) to control Pdgfrβ expression by p53-dependent and -independent mechanisms involving RNA transcription and protein synthesis, respectively, to promote the vascular remodeling needed for normal vision.
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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.