Evidence map›Paper›PMID 30679314›Full record

ArticleThe Journal of biological chemistry2019

EGF receptor and PKCδ kinase activate DNA damage-induced pro-survival and pro-apoptotic signaling via biphasic activation of ERK and MSK1 kinases.

Angela M Ohm, Trisiani Affandi, Mary E Reyland

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. 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
1.5field-weighted citation impact, top 17% 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, 26 citations in OpenAlex.

  1. Sensitive and Selective Next-Generation FRET-based PKA Biosensors.bioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. MAPK/ERK Pathway as a Central Regulator in Vertebrate Organ Regeneration.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Aging and Protein Kinases.Advances in experimental medicine and biology · 2021
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Targeting ERK-Hippo Interplay in Cancer Therapy.International journal of molecular sciences · 2020
    Review
  14. Article
  15. Article
  16. 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

3 authors at 1 institution in 1 country.

Angela M OhmFrom the Department of Craniofacial Biology, School of Dental Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80045.ORCID 0000-0002-4495-5103
Trisiani AffandiFrom the Department of Craniofacial Biology, School of Dental Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80045.ORCID 0000-0002-2307-0357
Mary E ReylandFrom the Department of Craniofacial Biology, School of Dental Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80045 Mary.Reyland@ucdenver.edu.
University of Colorado Anschutz Medical Campus · US

Funding

Regulation of Salivary Cell Apoptosis by Protein Kinase CR01DE015648 · NIDCR · UNIVERSITY OF COLORADO DENVER · PI REYLAND, MARY ELAINE · 2004 to 2019
$5.6M
Training Program in Cancer BiologyT32CA190216 · NCI · UNIVERSITY OF COLORADO DENVER · PI Craig T. Jordan · 2016 to 2026
$3.5M
PKCdelta and salivary gland radioprotectionR01DE027517 · NIDCR · UNIVERSITY OF COLORADO DENVER · PI REYLAND, MARY ELAINE · 2018 to 2022
$2.6M
NCI NIH HHS T32 CA190216NIDCR NIH HHS R01 DE015648NIDCR NIH HHS R01 DE027517
6 · The paper itself

Abstract

DNA damage-mediated activation of extracellular signal-regulated kinase (ERK) can regulate both cell survival and cell death. We show here that ERK activation in this context is biphasic and that early and late activation events are mediated by distinct upstream signals that drive cell survival and apoptosis, respectively. We identified the nuclear kinase mitogen-sensitive kinase 1 (MSK1) as a downstream target of both early and late ERK activation. We also observed that activation of ERK→MSK1 up to 4 h after DNA damage depends on epidermal growth factor receptor (EGFR), as EGFR or mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK)/ERK inhibitors or short hairpin RNA-mediated MSK1 depletion enhanced cell death. This prosurvival response was partially mediated through enhanced DNA repair, as EGFR or MEK/ERK inhibitors delayed DNA damage resolution. In contrast, the second phase of ERK→MSK1 activation drove apoptosis and required protein kinase Cδ (PKCδ) but not EGFR. Genetic disruption of PKCδ reduced ERK activation in an

Indexed as

ApoptosisCell SurvivalDNA DamageSignal TransductionEnzyme ActivationErbB ReceptorsExtracellular Signal-Regulated MAP KinasesHEK293 CellsHumansProtein Kinase C-deltaRibosomal Protein S6 Kinases, 90-kDaEGFR protein, humanErbB ReceptorsExtracellular Signal-Regulated MAP Kinasesmitogen and stress-activated protein kinase 1Protein Kinase C-deltaRibosomal Protein S6 Kinases, 90-kDaapoptosiscell signalingDNA damageepidermal growth factor receptor (EGFR)extracellular signal–regulated kinase (ERK)kinase cascademitogen-activated protein kinase (MAPK)mitogen-sensitive kinase (MSK)protein kinase C (PKC)signal transduction

Identifiers

PMID30679314
PMCPMC6433046
OpenAlexW2911569837

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.