Evidence map›Paper›PMID 35981542›Full record

ArticleMolecular cell2022

Chromatin-bound RB targets promoters, enhancers, and CTCF-bound loci and is redistributed by cell-cycle progression.

Ioannis Sanidas, Hanjun Lee, Purva H Rumde, Gaylor Boulay, Robert Morris, Gabriel Golczer, Marcelo Stanzione, Soroush Hajizadeh, Jun Zhong, Meagan B Ryan and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular cell, 2022. 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
–field-weighted citation impact
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.

  1. Article
  2. Article
  3. Chromatin association promotes UBR5-mediated degradation of Rb.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. The GScience advances · 2024
    Article
  12. Article
  13. Cancer takes many paths through G1/S.Trends in cell biology · 2024
    Review
  14. Review
  15. The G1/S transition is promoted by Rb degradation via the E3 ligase UBR5.bioRxiv : the preprint server for biology · 2024
    Article
  16. Article
  17. Review
  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

15 authors.

Ioannis SanidasMassachusetts General Hospital Cancer Center, Harvard Medical School, Building 149 13th Street, Charlestown, MA 02129, USA.
Hanjun LeeMassachusetts General Hospital Cancer Center, Harvard Medical School, Building 149 13th Street, Charlestown, MA 02129, USA; Broad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA; Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.
Purva H RumdeMassachusetts General Hospital Cancer Center, Harvard Medical School, Building 149 13th Street, Charlestown, MA 02129, USA.
Gaylor BoulayMassachusetts General Hospital Cancer Center, Harvard Medical School, Building 149 13th Street, Charlestown, MA 02129, USA; Broad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA.
Robert MorrisMassachusetts General Hospital Cancer Center, Harvard Medical School, Building 149 13th Street, Charlestown, MA 02129, USA.
Gabriel GolczerMassachusetts General Hospital Cancer Center, Harvard Medical School, Building 149 13th Street, Charlestown, MA 02129, USA.
Marcelo StanzioneMassachusetts General Hospital Cancer Center, Harvard Medical School, Building 149 13th Street, Charlestown, MA 02129, USA.
Soroush HajizadehMassachusetts General Hospital Cancer Center, Harvard Medical School, Building 149 13th Street, Charlestown, MA 02129, USA.
Jun ZhongMassachusetts General Hospital Cancer Center, Harvard Medical School, Building 149 13th Street, Charlestown, MA 02129, USA.
Meagan B RyanMassachusetts General Hospital Cancer Center, Harvard Medical School, Building 149 13th Street, Charlestown, MA 02129, USA.
Ryan B CorcoranMassachusetts General Hospital Cancer Center, Harvard Medical School, Building 149 13th Street, Charlestown, MA 02129, USA.
Benjamin J DrapkinMassachusetts General Hospital Cancer Center, Harvard Medical School, Building 149 13th Street, Charlestown, MA 02129, USA; UT Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390, USA.
Miguel N RiveraMassachusetts General Hospital Cancer Center, Harvard Medical School, Building 149 13th Street, Charlestown, MA 02129, USA; Broad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA.
Nicholas J DysonMassachusetts General Hospital Cancer Center, Harvard Medical School, Building 149 13th Street, Charlestown, MA 02129, USA. Electronic address: dyson@helix.mgh.harvard.edu.
Michael S LawrenceMassachusetts General Hospital Cancer Center, Harvard Medical School, Building 149 13th Street, Charlestown, MA 02129, USA; Broad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA. Electronic address: lawrence@broadinstitute.org.

Funding

Using patient-derived models to understand drug responses in SCLCU01CA220323 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI DYSON, NICHOLAS J · 2018 to 2022
$3.1M
Deciphering the code of RB phosphorylationR01CA236538 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI DYSON, NICHOLAS J · 2018 to 2022
$2.5M
The consequences of RB-lossR01GM117413 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI DYSON, NICHOLAS J · 2016 to 2019
$2.1M
Dissecting and overcoming cross-resistance to DNA damaging agents in SCLCK08CA237832 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI DRAPKIN, BENJAMIN J · 2020 to 2024
$1.2M
NCI NIH HHS K08 CA237832NCI NIH HHS R01 CA236538NCI NIH HHS U01 CA220323NIGMS NIH HHS R01 GM117413
6 · The paper itself

Abstract

The interaction of RB with chromatin is key to understanding its molecular functions. Here, for first time, we identify the full spectrum of chromatin-bound RB. Rather than exclusively binding promoters, as is often described, RB targets three fundamentally different types of loci (promoters, enhancers, and insulators), which are largely distinguishable by the mutually exclusive presence of E2F1, c-Jun, and CTCF. While E2F/DP facilitates RB association with promoters, AP-1 recruits RB to enhancers. Although phosphorylation in CDK sites is often portrayed as releasing RB from chromatin, we show that the cell cycle redistributes RB so that it enriches at promoters in G1 and at non-promoter sites in cycling cells. RB-bound promoters include the classic E2F-targets and are similar between lineages, but RB-bound enhancers associate with different categories of genes and vary between cell types. Thus, RB has a well-preserved role controlling E2F in G1, and it targets cell-type-specific enhancers and CTCF sites when cells enter S-phase.

Indexed as

ChromatinRetinoblastoma ProteinCell Cycle ProteinsE2F1 Transcription FactorE2F Transcription FactorsPromoter Regions, GeneticTranscription Factor AP-1Cell Cycle ProteinsChromatinE2F1 Transcription FactorE2F Transcription FactorsRetinoblastoma ProteinTranscription Factor AP-1AP-1cell-cycle regulationCTCFE2FPanChIPRB-bound enhancersRB-bound promotersRB phosphorylationregulation of RB activityretinoblastoma protein

Identifiers

PMID35981542
PMCPMC9481721

What OpenQuestion holds

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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.