Evidence map›Paper›PMID 18794805›Full record

ArticleOncogene2009

Phosphorylation by p38 MAP kinase is required for E2F1 degradation and keratinocyte differentiation.

I A Ivanova, K-A Nakrieko, L Dagnino

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 34 citations in OpenAlex.

  1. Calcineurin-mediated dephosphorylation stabilizes E2F1 protein by suppressing binding of the FBXW7 ubiquitin ligase subunit.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  2. Regulation of E2F1 activity via PKA-mediated phosphorylations.Turkish journal of biology = Turk biyoloji dergisi · 2020
    Article
  3. Article
  4. Article
  5. Regulation of E2F1 Transcription Factor by Ubiquitin Conjugation.International journal of molecular sciences · 2017
    Review
  6. EGFR Induces E2F1-Mediated Corticotroph Tumorigenesis.Journal of the Endocrine Society · 2017
    Article
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  11. Review
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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

3 authors at 3 institutions in 2 countries.

I A IvanovaDepartment of Physiology and Pharmacology, and Regulatory Biology and Functional Genomics Research Group, Siebens-Drake Research Institute, University of Western Ontario, London, ON, Canada.
K-A Nakrieko
L Dagnino
Lawson Health Research Institute · CAUniversity Medical Center Utrecht · NLWestern University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor E2F1 plays key roles in skin homeostasis, and is essential for normal keratinocyte proliferation and epidermal regeneration after injury. We have previously established that, in differentiating keratinocytes, E2F1 activity is controlled by nuclear export and subsequent degradation. These events are triggered by differentiation-induced stimulation of protein kinase C and p38 mitogen-activated protein kinase (MAPK). However, the mechanisms that induce E2F1 export from the nucleus and the role of p38 MAPK in this process are poorly understood. We now describe a novel regulatory pathway for E2F1, which involves phosphorylation by p38. We demonstrate that E2F1 forms complexes with active p38 through regions that exclude the N-terminus of this transcription factor, and that p38 activity is a major contributor to the phosphorylation status of E2F1 in keratinocytes. Using in vitro kinase assays, we identified Ser403 and Thr433 as the residues phosphorylated by p38. The biological significance of these observations is underscored by the inability of E2F1 mutants lacking one or both of these residues to be exported from the nucleus and degraded when keratinocytes receive differentiation stimuli, which results in impaired keratinocyte maturation.

Indexed as

Cell DifferentiationAnimalsCell LineDNA Mutational AnalysisE2F1 Transcription FactorKeratinocytesMicep38 Mitogen-Activated Protein KinasesPhosphorylationSequence DeletionSerineThreonineE2f1 protein, mouseE2F1 Transcription Factorp38 Mitogen-Activated Protein KinasesSerineThreonine

Identifiers

PMID18794805
OpenAlexW2019897778

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.