Evidence map›Paper›PMID 29981477›Full record

ArticleBiochimica et biophysica acta. Gene regulatory mechanisms2018

Poly(ADP-ribosyl)ation associated changes in CTCF-chromatin binding and gene expression in breast cells.

Ioanna Pavlaki, France Docquier, Igor Chernukhin, Georgia Kita, Svetlana Gretton, Christopher T Clarkson, Vladimir B Teif, Elena Klenova

Open access · hybridAbstract read
In one paragraph

Article in Biochimica et biophysica acta. Gene regulatory mechanisms, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. 3D genome alterations and editing in pathology.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Review
  6. Review
  7. Review
  8. CTCF: A misguided jack-of-all-trades in cancer cells.Computational and structural biotechnology journal · 2022
    Review
  9. Regulation of 3D chromatin organization by CTCF.Current opinion in genetics & development · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. 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.

Ioanna PavlakiUniversity of Essex, School of Biological Sciences, Wivenhoe Park, Colchester, Essex CO4 3SQ, UK.
France DocquierUniversity of Essex, School of Biological Sciences, Wivenhoe Park, Colchester, Essex CO4 3SQ, UK.
Igor ChernukhinUniversity of Essex, School of Biological Sciences, Wivenhoe Park, Colchester, Essex CO4 3SQ, UK.
Georgia KitaUniversity of Essex, School of Biological Sciences, Wivenhoe Park, Colchester, Essex CO4 3SQ, UK.
Svetlana GrettonUniversity of Essex, School of Biological Sciences, Wivenhoe Park, Colchester, Essex CO4 3SQ, UK.
Christopher T ClarksonUniversity of Essex, School of Biological Sciences, Wivenhoe Park, Colchester, Essex CO4 3SQ, UK.
Vladimir B TeifUniversity of Essex, School of Biological Sciences, Wivenhoe Park, Colchester, Essex CO4 3SQ, UK. Electronic address: vteif@essex.ac.uk.
Elena KlenovaUniversity of Essex, School of Biological Sciences, Wivenhoe Park, Colchester, Essex CO4 3SQ, UK. Electronic address: klenovae@essex.ac.uk.
University of Essex · GB

Funding

Medical Research Council G0401088Wellcome Trust
6 · The paper itself

Abstract

CTCF is an evolutionarily conserved and ubiquitously expressed architectural protein regulating a plethora of cellular functions via different molecular mechanisms. CTCF can undergo a number of post-translational modifications which change its properties and functions. One such modifications linked to cancer is poly(ADP-ribosyl)ation (PARylation). The highly PARylated CTCF form has an apparent molecular mass of 180 kDa (referred to as CTCF180), which can be distinguished from hypo- and non-PARylated CTCF with the apparent molecular mass of 130 kDa (referred to as CTCF130). The existing data accumulated so far have been mainly related to CTCF130. However, the properties of CTCF180 are not well understood despite its abundance in a number of primary tissues. In this study we performed ChIP-seq and RNA-seq analyses in human breast cells 226LDM, which display predominantly CTCF130 when proliferating, but CTCF180 upon cell cycle arrest. We observed that in the arrested cells the majority of sites lost CTCF, whereas fewer sites gained CTCF or remain bound (i.e. common sites). The classical CTCF binding motif was found in the lost and common, but not in the gained sites. The changes in CTCF occupancies in the lost and common sites were associated with increased chromatin densities and altered expression from the neighboring genes. Based on these results we propose a model integrating the CTCF130/180 transition with CTCF-DNA binding and gene expression changes. This study also issues an important cautionary note concerning the design and interpretation of any experiments using cells and tissues where CTCF180 may be present.

Indexed as

Gene ExpressionPoly ADP RibosylationBreastCCCTC-Binding FactorCell LineChromatinDNAFemaleHumansHydroxyureaNocodazoleNucleosomesNucleotide MotifsCCCTC-Binding FactorChromatinCTCF protein, humanDNAHydroxyureaNocodazoleNucleosomes

Identifiers

PMID29981477
PMCPMC6074063
OpenAlexW2953332656

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.