Evidence map›Paper›PMID 22354964›Full record

ArticleThe Journal of biological chemistry2012

De-SUMOylation of CCCTC binding factor (CTCF) in hypoxic stress-induced human corneal epithelial cells.

Jie Wang, Yumei Wang, Luo Lu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Regulation of 3D chromatin organization by CTCF.Current opinion in genetics & development · 2021
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. SUMO: a (oxidative) stressed protein.Neuromolecular medicine · 2013
    Review
  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

3 authors at 1 institution in 1 country.

Jie WangDepartment of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Torrance, California 90502, USA.
Yumei Wang
Luo Lu
University 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
Differential Effects of Corneal Hypoxia on Limbal Stem and Epithelial Cell FatesR01EY022364 · NEI · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI LU, LUO · 2012 to 2016
$1.6M
NEI NIH HHS R01 EY015281NEI NIH HHS R01-EY015282NEI NIH HHS R01 EY022364
6 · The paper itself

Abstract

Epigenetic factor CCCTC binding factor (CTCF) plays important roles in the genetic control of cell fate. Previous studies found that CTCF is positively and negatively regulated at the transcriptional level by epidermal growth factor (EGF) and ultraviolet (UV) stimulation, respectively. However, it is unknown whether other stresses modify the CTCF protein. Here, we report that regulation of CTCF by de-SUMOylation is dependent upon hypoxic and oxidative stresses. We found that stimulation of human corneal epithelial cells with hypoxic stress suppressed a high molecular mass form of CTCF (150 kDa), but not a lower molecular weight form of CTCF (130 kDa). Further investigation revealed that the hypoxic stress-suppressed 150-kDa CTCF was a small ubiquitin-related modifier (SUMO)ylated form of the protein. Hypoxic stress-induced de-SUMOylation of human CTCF was associated with lysine 74 and 689 residues, but not to the phosphorylation of CTCF. Overexpression of SENP1 induced de-SUMOylation of CTCF. However, knockdown of SENP1 could not rescue hypoxic stress-induced CTCF de-SUMOylation. Overexpression of SUMO1 and SUMO2 increased SUMOylation of CTCF and partially blocked hypoxic stress-induced CTCF de-SUMOylation, suggesting that free cellular SUMO proteins play roles in regulating hypoxia-induced CTCF de-SUMOylation. In addition, hypoxic stress significantly inhibited PAX6 mRNA and protein expressions by suppression of PAX6-P0 promoter activity. The result was further supported by data showing that knockdown of CTCF significantly enhanced expression of PAX6 and abolished hypoxia-induced suppression of PAX6. Thus, we conclude that hypoxic stress induces de-SUMOylation of CTCF to functionally regulate CTCF activity.

Indexed as

Protein Processing, Post-TranslationalCCCTC-Binding FactorCell HypoxiaCells, CulturedCorneaCysteine EndopeptidasesEndopeptidasesEpithelial CellsEye ProteinsGene ExpressionGene Expression RegulationHomeodomain ProteinsHumansMolecular WeightOxidative StressPaired Box Transcription FactorsCCCTC-Binding FactorCTCF protein, humanCysteine EndopeptidasesEndopeptidasesEye ProteinsHomeodomain ProteinsPaired Box Transcription FactorsPAX6 protein, humanPAX6 Transcription FactorRepressor ProteinsSENP1 protein, human

Identifiers

PMID22354964
PMCPMC3320996
OpenAlexW2054720349

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.