Evidence map›Paper›PMID 14511403›Full record

ArticleNeoplasia (New York, N.Y.)

The role of JNK and p38 MAPK activities in UVA-induced signaling pathways leading to AP-1 activation and c-Fos expression.

Amy L Silvers, Michael A Bachelor, G Timothy Bowden

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
6.5field-weighted citation impact, top 4% 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

51 citing papers in PubMed, 120 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Antioxidants (Basel, Switzerland) · 2024
    Article
  10. Annals of dermatology · 2024
    Article
  11. Review
  12. Article
  13. Article
  14. Acacetin resists UVA photoaging by mediating the SIRT3/ROS/MAPKs pathway.Journal of cellular and molecular medicine · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Role of Phytochemicals in Skin PhotoprotectionFrontiers in pharmacology · 2022
    Review
  19. Article
  20. Antioxidant and Anti-Inflammatory Effects ofAntioxidants (Basel, Switzerland) · 2021
    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.

Amy L SilversDepartment of Radiation Oncology, Arizona Cancer Center, The University of Arizona, Tucson, AZ, USA.
Michael A Bachelor
G Timothy Bowden
University of Arizona · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
VITAMIN A, AND ITS PRECURSORS AND DERIVATIVES AS THERAPEUTIC MODALITIESP01CA027502 · NCI · UNIVERSITY OF ARIZONA · PI EINSPAHR, JANINE G · 1985 to 2015
$36.3M
Cancer Prevention and Control Translational ResearchR25CA078447 · NCI · UNIVERSITY OF ARIZONA · PI ALBERTS, DAVID SAMUEL · 1998 to 2014
$7.6M
NCI NIH HHS CA23074NCI NIH HHS CA27502NCI NIH HHS P01 CA027502NCI NIH HHS P30 CA023074NCI NIH HHS R25 CA078447NCI NIH HHS R25CA78447
6 · The paper itself

Abstract

To further delineate ultraviolet A (UVA) signaling pathways in the human keratinocyte cell line HaCaT, we examined the potential role of mitogen-activated protein kinases (MAPKs) in UVA-induced activator protein-1 (AP-1) transactivation and c-Fos expression. UVA-induced phosphorylation of p38 and c-Jun N-terminal kinase (JNK) proteins was detected immediately after irradiation and disappeared after approximately 2 hours. Conversely, phosphorylation of extracellular signal-regulated kinase was significantly inhibited for up to 1 hour post-UVA irradiation. To examine the role of p38 and JNK MAPKs in UVA-induced AP-1 and c-fos transactivations, the selective pharmacologic MAPK inhibitors, SB202190 (p38 inhibitor) and SP600125 (JNK inhibitor), were used to independently treat stably transfected HaCaT cells in luciferase reporter assays. Both SB202190 and SP600125 dose-dependently inhibited UVA-induced AP-1 and c-fos transactivations. SB202190 (0.25-0.5 microM) and SP600125 (62-125 nM) treatments also primarily inhibited UVA-induced c-Fos expression. These results demonstrated that activation of both JNK and p38 play critical role in UVA-mediated AP-1 transactivation and c-Fos expression in these human keratinocyte cells. Targeted inhibition of these MAPKs with their selective pharmacologic inhibitors may be effective chemopreventive strategies for UVA-induced nonmelanoma skin cancer.

Indexed as

JNK Mitogen-Activated Protein KinasesSignal TransductionAnthracenesBlotting, WesternCell LineDose-Response Relationship, DrugEnzyme ActivationEnzyme InhibitorsHumansImidazolesLuciferasesMAP Kinase Kinase 4Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesPhosphorylation4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazoleAnthracenesEnzyme InhibitorsImidazolesJNK Mitogen-Activated Protein KinasesLuciferasesMAP Kinase Kinase 4Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-fospyrazolanthronePyridinesTranscription Factor AP-1

Identifiers

PMID14511403
PMCPMC1502419
OpenAlexW1981123168

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.