Evidence map›Paper›PMID 21172820›Full record

ArticleJournal of cell science2011

TbetaRI/Alk5-independent TbetaRII signaling to ERK1/2 in human skin cells according to distinct levels of TbetaRII expression.

Balaji Bandyopadhyay, Arum Han, Jinyao Dai, Jianhua Fan, Yong Li, Mei Chen, David T Woodley, Wei Li

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

23 citing papers in PubMed, 45 citations in OpenAlex.

  1. SMURF2 in Anticancer Therapy: Dual Role in Carcinogenesis and Theranostics.International journal of molecular sciences · 2026
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  13. Non-Smad Signaling Pathways of the TGF-β Family.Cold Spring Harbor perspectives in biology · 2017
    Review
  14. Signaling Receptors for TGF-β Family Members.Cold Spring Harbor perspectives in biology · 2016
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 1 institution in 1 country.

Balaji BandyopadhyayThe Department of Dermatology and the USC-Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, CA 90033, USA.
Arum Han
Jinyao Dai
Jianhua Fan
Yong Li
Mei Chen
David T Woodley
Wei Li
University of Southern California · US

Funding

PURIFICATION OF EPIDERMOLYSIS BULLOSA ANTIGENR01AR033625 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHEN, MEI, WOODLEY, DAVID T. · 1986 to 2012
$4.8M
MECHANISMS OF KERATINOCYTE MOTILITYR01AR046538 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI WOODLEY, DAVID T. · 1999 to 2009
$3.2M
NIAMS NIH HHS AR46538NIAMS NIH HHS GM/AR67100-01NIAMS NIH HHS R01 AR033625NIAMS NIH HHS R01 AR046538
6 · The paper itself

Abstract

TGFβ binding to the TGFβ receptor (TβR) activates R-Smad-dependent pathways, such as Smad2/3, and R-Smad-independent pathways, such as ERK1/2. The mechanism of the TGFβ-TβRII-TβRI-Smad2/3 pathway is established; however, it is not known how TGFβ activates ERK1/2. We show here that although TGFβ equally activated Smad2/3 in all cells, it selectively activated ERK1/2 in dermal cells and inhibited ERK1/2 in epidermal cells. These opposite effects correlated with the distinct expression levels of TβRII, which are 7- to 18-fold higher in dermal cells than in epidermal cells. Reduction of TβRII expression in dermal cells abolished TGFβ-stimulated ERK1/2 activation. Upregulation of TβRII expression in epidermal cells to a similar level as that in dermal cells switched TGFβ-induced ERK1/2 inhibition to ERK1/2 activation. More intriguingly, in contrast to the equal importance of TβRII in mediating TGFβ signaling to both Smad2/3 and ERK1/2, knockdown of TβRI/Alk5 blocked activation of only Smad2/3, not ERK1/2, in dermal cells. Similarly, expression of the constitutively activated TβRI-TD kinase activated only Smad2/3 and not ERK1/2 in epidermal cells. This study provides an explanation for why TGFβ selectively activates ERK1/2 in certain cell types and direct evidence for TβRI-independent TβRII signaling to a R-Smad-independent pathway.

Indexed as

Signal TransductionCell LineCells, CulturedDermisEpidermal CellsEpidermisGene ExpressionHumansMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Protein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IReceptor, Transforming Growth Factor-beta Type IISmad2 ProteinTransforming Growth Factor betaMAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Protein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IReceptor, Transforming Growth Factor-beta Type IISmad2 ProteinSMAD2 protein, humanTGFBR1 protein, humanTransforming Growth Factor beta

Identifiers

PMID21172820
PMCPMC3001406
OpenAlexW2092621683

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.