Evidence map›Paper›PMID 11840343›Full record

ArticleOncogene2002

Regulation of p73 by c-Abl through the p38 MAP kinase pathway.

Ricardo Sanchez-Prieto, Victor Javier Sanchez-Arevalo, Joan-Marc Servitja, J Silvio Gutkind

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 109 citations in OpenAlex.

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  14. AMPK couples p73 with p53 in cell fate decision.Cell death and differentiation · 2014
    Article
  15. Article
  16. Article
  17. Overactivation of mitogen-activated protein kinase and suppression of mitofusin-2 expression are two independent events in high mobility group box 1 protein-mediated T cell immune dysfunction.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2013
    Article
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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

4 authors at 2 institutions in 2 countries.

Ricardo Sanchez-PrietoOral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4330, USA.
Victor Javier Sanchez-Arevalo
Joan-Marc Servitja
J Silvio Gutkind
National Institute of Dental and Craniofacial Research · USHospital Universitario Puerta de Hierro Majadahonda · ES

Funding

Molecular Mechanisms Of Growth Control And CarcinogenesisZIADE000551 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI GUTKIND, JORGE SILVIO · 2009 to 2015
$11.5M
Oral CarcinogenesisZIADE000558 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI GUTKIND, JORGE SILVIO · 2009 to 2015
$11.4M
ORAL CARCINOGENESISZ01DE000558 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI GUTKIND, J · 1992 to 2008
$3.6M
ROLE OF G PROTEINS IN GROWTH CONTROL AND CARCINOGENESISZ01DE000551 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI GUTKIND, J · 1992 to 2008
$3.4M
6 · The paper itself

Abstract

p73 is a novel member of the p53 family of tumor suppressor proteins which is involved in cellular differentiation, tumor suppression, and the response to genotoxic stress. The molecular mechanisms regulating p73 activity are still poorly understood. Recently, p73 was found to be a target of the enzymatic activity of c-Abl, a non-receptor tyrosine kinase that potently activated in response to DNA damage. Here, we present evidence that c-Abl induces the phosphorylation of p73 in threonine residues adjacent to prolines, and that the p38 MAP kinase pathway mediates this response. Furthermore, we found that activation of p38 is sufficient to enhance the stability of p73, and that the transcriptional activation of p73 by c-Abl requires the activity of p38. These findings indicate that members of the MAP kinases superfamily of signaling molecules can regulate p73, and support a role for the p38 MAP kinase in a novel biochemical pathway by which c-Abl regulates this p53-related molecule.

Indexed as

Genes, ablMAP Kinase Signaling SystemBone NeoplasmsCalcium-Calmodulin-Dependent Protein KinasesCell LineDNA-Binding ProteinsEnzyme ActivationEnzyme InhibitorsEpithelial CellsGenes, Tumor SuppressorHumansImidazolesJNK Mitogen-Activated Protein KinasesKidneyMAP Kinase Kinase 1MAP Kinase Kinase 6Calcium-Calmodulin-Dependent Protein KinasesDNA-Binding ProteinsEnzyme InhibitorsImidazolesJNK Mitogen-Activated Protein KinasesMAP2K1 protein, humanMAP2K6 protein, humanMAP2K7 protein, humanMAP Kinase Kinase 1MAP Kinase Kinase 6MAP Kinase Kinase 7Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesNuclear Proteinsp38 Mitogen-Activated Protein KinasesPhosphoserinePhosphotyrosineProlineProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins c-ablPyridinesRecombinant Fusion ProteinsSB 203580TP73 protein, humanTumor Protein p73Tumor Suppressor Proteins

Identifiers

PMID11840343
OpenAlexW2316798217

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.