Evidence map›Paper›PMID 20110362›Full record

ArticleThe Journal of biological chemistry2010

NF-kappaB subtypes regulate CCCTC binding factor affecting corneal epithelial cell fate.

Luo Lu, Ling Wang, Tie Li, Jie Wang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

19 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
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  7. Article
  8. Progress in corneal wound healing.Progress in retinal and eye research · 2015
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Dependence of corneal epithelial cell proliferation on modulation of interactions between ERK1/2 and NKCC1.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2011
    Article
  19. Role of CTCF in DNA damage response.Mutation research. Reviews in mutation research
    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

4 authors at 2 institutions in 1 country.

Luo LuDepartment of Medicine, David Geffen School of Medicine, University of California Los Angeles, Torrance, California 90502. Electronic address: lluou@ucla.edu.
Ling WangDepartment of Medicine, David Geffen School of Medicine, University of California Los Angeles, Torrance, California 90502.
Tie LiDepartment of Medicine, David Geffen School of Medicine, University of California Los Angeles, Torrance, California 90502.
Jie WangDepartment of Medicine, David Geffen School of Medicine, University of California Los Angeles, Torrance, California 90502.
University of California, Los Angeles · USUniversity of California System · US

Funding

Role of CTCF in EGF_Induced Corneal Epithelial GrowthR01EY015281 · NEI · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI LU, LUO · 2004 to 2014
$3.0M
NEI NIH HHS R01 EY015281NEI NIH HHS R01-EY015282
6 · The paper itself

Abstract

CCCTC binding factor (CTCF) controls DNA imprinting, insulates important gene expression, and mediates growth factor- and stress-induced cell fate. However, regulatory mechanisms involved in intracellular CTCF activity are largely unknown. In this study, we show that epidermal growth factor (EGF)-induced increase and UV stress-induced decrease in CTCF activities mediate human corneal epithelial cell proliferation and apoptosis, respectively. CTCF is regulated by activation of different NF-kappaB subtypes via stimulation by EGF and UV stress. EGF-induced formation of a p65/p50 heterodimer activated CTCF transcription to promote cellular proliferation. This was accomplished by the heterodimer binding to a kappaB site in the promoter region of CTCF gene. In contrast, UV stress induced formation of a p50/p50 homodimer, which suppressed CTCF expression leading to apoptosis. Thus, CTCF by itself plays a central role in mediating the dichotomous effects of growth factor- and stress-stimulated NF-kappaB activation on cell survival and death. These results suggest that CTCF is a downstream component of the NF-kappaB pathway involved in the core transcriptional network of cell fate.

Indexed as

Active Transport, Cell NucleusCCCTC-Binding FactorCell DeathCell LineageCell ProliferationCell SurvivalDimerizationEpidermal Growth FactorEpithelial CellsHumansNF-kappa BPromoter Regions, GeneticProtein BindingRepressor ProteinsTranscription, GeneticUltraviolet RaysCCCTC-Binding FactorCTCF protein, humanEpidermal Growth FactorNF-kappa BRepressor Proteins

Identifiers

PMID20110362
PMCPMC2843186
OpenAlexW2015285056

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.