ArticleOncogene2003
Function of p73, not of p53, is inhibited by the physical interaction with RACK1 and its inhibitory effect is counteracted by pRB.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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
18 citing papers in PubMed, 48 citations in OpenAlex.
- A Duality of Function: An Integrative Model of RACK1 as a Switch Between Translational and Signaling Hubs.International journal of molecular sciences · 2025Review
- Review
- p53, p63 and p73 in the wonderland ofOncotarget · 2017Review
- The association of receptor of activated protein kinase C 1(RACK1) with infectious bursal disease virus viral protein VP5 and voltage-dependent anion channel 2 (VDAC2) inhibits apoptosis and enhances viral replication.The Journal of biological chemistry · 2015Article
- A nanotechnological, molecular-modeling, and immunological approach to study the interaction of the anti-tumorigenic peptide p28 with the p53 family of proteins.International journal of nanomedicine · 2014Article
- RACK1 to the future--a historical perspective.Cell communication and signaling : CCS · 2013Article
- TAp73alpha protects small cell lung carcinoma cells from caspase-2 induced mitochondrial mediated apoptotic cell death.Oncotarget · 2011Article
- Hsp72 mediates TAp73α anti-apoptotic effects in small cell lung carcinoma cells.Journal of cellular and molecular medicine · 2011Article
- RACK-1 overexpression protects against goniothalamin-induced cell death.Toxicology letters · 2009Article
- Stxbp4 regulates DeltaNp63 stability by suppression of RACK1-dependent degradation.Molecular and cellular biology · 2009Article
- Cataloging and organizing p73 interactions in cell cycle arrest and apoptosis.Nucleic acids research · 2008Article
- RACK1 and CIS mediate the degradation of BimEL in cancer cells.The Journal of biological chemistry · 2008Article
- Acetylcholinesterase-R increases germ cell apoptosis but enhances sperm motility.Journal of cellular and molecular medicine · 2008Article
- Regulation of p73 by Hck through kinase-dependent and independent mechanisms.BMC molecular biology · 2007Article
- Ubiquitin and ubiquitin-like modifications of the p53 family.Neoplasia (New York, N.Y.) · 2006Review
- p73, a sophisticated p53 family member in the cancer world.Cancer science · 2005Review
- Protein stability and function of p73 are modulated by a physical interaction with RanBPM in mammalian cultured cells.Oncogene · 2005Article
- Yeast Asc1p and mammalian RACK1 are functionally orthologous core 40S ribosomal proteins that repress gene expression.Molecular and cellular biology · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The newly identified p53-related gene, p73, encodes a nuclear transcription factor. Unlike p53, p73 has various isoforms with different NH(2)- and COOH-terminal tails. p73alpha with the longest COOH-terminal extension is most abundantly expressed in many tissues and cells among those splicing isoforms of p73 and the COOH-terminal region appears to have an autoregulatory function. To isolate and characterize the cellular protein(s) that interacts with the unique COOH-terminal region of p73alpha, we employed a yeast two-hybrid screen with a human fetal brain and 293 cell cDNA libraries. We identified the receptor for activated C kinase (RACK1) as a new member of p73alpha-binding proteins. The interaction was confirmed by coimmunoprecipitation experiments, whereas RACK1 did not interact with p53 or p73beta. Ectopic overexpression of RACK1 in SAOS-2 cells reduced the p73alpha-mediated transcription from the p53/p73-responsive promoters, and inhibited the p73alpha-dependent apoptosis. On the other hand, the p53-dependent transcriptional activation as well as apoptosis was unaffected in the presence of RACK1. Furthermore, we found that pRB physically bound to RACK1, and repressed the RACK1-dependent inhibition of p73alpha. Taken together, our observations suggest that pRB diminishes the RACK1-mediated inhibition of p73alpha activity through the interaction with RACK1.
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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.