Evidence map›Paper›PMID 22982089›Full record

ArticleCellular signalling2013

Cellular retinoic acid binding protein I mediates rapid non-canonical activation of ERK1/2 by all-trans retinoic acid.

Shawna D Persaud, Yi-Wei Lin, Cheng-Ying Wu, Hiroyuki Kagechika, Li-Na Wei

Open access · greenAbstract read
In one paragraph

Article in Cellular signalling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

42 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. CRABP1-complexes in exosome secretion.Cell communication and signaling : CCS · 2024
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Retinoid metabolism: new insights.Journal of molecular endocrinology · 2022
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Biomarkers in retinoblastoma.International journal of ophthalmology · 2020
    Review
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

5 authors at 2 institutions in 2 countries.

Shawna D PersaudDepartment of Pharmacology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.
Yi-Wei Lin
Cheng-Ying Wu
Hiroyuki Kagechika
Li-Na Wei
University of Minnesota Medical Center · USTokyo Medical and Dental University · JP

Funding

Studies of nuclear receptor corepressor, NRIP1, in vitamin A signaling pathwaysR01DK060521 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI WEI, LI-NA · 2002 to 2022
$6.9M
TR2 NUCLEAR RECEPTOR IN VITAMIN A SIGNALING PATHWAYSR01DK054733 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI WEI, LI-NA · 1999 to 2021
$5.7M
Studies of the Mouse Kappa Opioid Receptor GeneK02DA013926 · NIDA · UNIVERSITY OF MINNESOTA TWIN CITIES · PI WEI, LI-NA · 2002 to 2011
$1.2M
NIDA NIH HHS K02 DA013926NIDA NIH HHS K02-DA13926NIDDK NIH HHS DK54733NIDDK NIH HHS DK60521NIDDK NIH HHS R01 DK054733NIDDK NIH HHS R01 DK060521
6 · The paper itself

Abstract

All-trans retinoic acid (atRA), one of the active ingredients of vitamin A, exerts canonical activities to regulate gene expression mediated by nuclear RA receptors (RARs). AtRA could also elicit certain non-canonical activities including, mostly, rapid activation of extracellular signal regulated kinase 1/2 (ERK1/2); but the mechanism was unclear. In this study, we have found that cellular retinoic acid binding protein I (CRABPI) mediates the non-canonical, RAR- and membrane signal-independent activation of ERK1/2 by atRA in various cellular backgrounds. In the context of embryonic stem cells (ESCs), atRA/CRABPI-dependent ERK1/2 activation rapidly affects ESC cell cycle, specifically to expand the G1 phase. This is mediated by ERK stimulation resulting in dephosphorylation of nuclear p27, which elevates nuclear p27 protein levels to block G1 progression to S phase. This is the first study to identify CRABPI as the mediator for non-canonical activation of ERK1/2 by atRA, and demonstrate a new functional role for CRABPI in modulating ESC cell cycle progression.

Indexed as

AnimalsAntineoplastic AgentsCell LineCell NucleusChlorocebus aethiopsCOS CellsCyclin-Dependent Kinase Inhibitor p27Embryonic Stem CellsEnzyme ActivationG1 Phase Cell Cycle CheckpointsMiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Receptors, Retinoic AcidRNA InterferenceRNA, Small InterferingAntineoplastic AgentsCyclin-Dependent Kinase Inhibitor p27Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Receptors, Retinoic Acidretinoic acid binding protein I, cellularRNA, Small InterferingTretinoin

Identifiers

PMID22982089
PMCPMC3508141
OpenAlexW2147034045

What OpenQuestion holds

Textmetadata
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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.