Evidence map›Paper›PMID 18612801›Full record

ArticleMolecular and cellular biochemistry2008

Ubiquitin over-expression promotes E6AP autodegradation and reactivation of the p53/MDM2 pathway in HeLa cells.

Rita Crinelli, Marzia Bianchi, Michele Menotta, Elisa Carloni, Elisa Giacomini, Marzia Pennati, Mauro Magnani

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Ubiquitin E3 Ligases and p53 in Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2025
    Review
  2. Article
  3. The Ubiquitin Gene Expression Pattern and Sensitivity toInternational journal of molecular sciences · 2020
    Article
  4. Article
  5. Induction ofFEBS open bio · 2018
    Article
  6. The Autism Protein Ube3A/E6AP Remodels Neuronal Dendritic Arborization via Caspase-Dependent Microtubule Destabilization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  7. Article
  8. Article
  9. Evaluation of selected binding domains for the analysis of ubiquitinated proteomes.Journal of the American Society for Mass Spectrometry · 2013
    Article
  10. Article
  11. Article
  12. Article
  13. YY1 is a novel potential therapeutic target for the treatment of HPV infection-induced cervical cancer by arsenic trioxide.International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2011
    Article
  14. Review
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Rita CrinelliIstituto di Chimica Biologica G. Fornaini, Università degli Studi di Urbino Carlo Bo, via Saffi, 2, 61029 Urbino, PU, Italy. rita.crinelli@uniurb.it
Marzia Bianchi
Michele Menotta
Elisa Carloni
Elisa Giacomini
Marzia Pennati
Mauro Magnani
University of Urbino · ITFondazione IRCCS Istituto Nazionale dei Tumori · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been established that intracellular ubiquitin pools are subject to regulatory constrains. Less certain is the mechanism by which the pool of conjugated ubiquitin shift in parallel with total ubiquitin, and how this type of regulation affects the flux of substrates through the pathway. In this study we demonstrate that ubiquitin over-expression promotes the destabilization of the ubiquitin protein ligase E6AP, by a mechanism involving self-ubiquitination, and the stabilization of p53. These results represent the very first evidence that the levels of a ubiquitin ligase can be regulated in vivo by ubiquitin abundance, supporting the idea that a strict interrelationship between pathway component activities and ubiquitin pool size exists. Interestingly, ubiquitin-induced p53 accumulation did not induce cell-cycle arrest, suggesting that although fluctuations of the intracellular ubiquitin content may actively modulate the level of regulatory proteins, this event is not per se sufficient to elicit a cellular response in terms of proliferation.

Indexed as

Protein Processing, Post-TranslationalCatalytic DomainCell CycleCell NucleusCyclin-Dependent Kinase Inhibitor p21HeLa CellsHumansMutant ProteinsPhosphorylationProtein TransportProto-Oncogene Proteins c-mdm2ThermodynamicsTranscriptional ActivationTranscription, GeneticTransfectionTumor Suppressor Protein p53Cyclin-Dependent Kinase Inhibitor p21MDM2 protein, humanMutant ProteinsProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53UBE3A protein, humanUbiquitinUbiquitin-Protein Ligases

Identifiers

PMID18612801
OpenAlexW2032459623

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.