Evidence map›Paper›PMID 30902546›Full record

ArticleMolecular cell2019

Gene-Specific H1 Eviction through a Transcriptional Activator→p300→NAP1→H1 Pathway.

Miho Shimada, Wei-Yi Chen, Tomoyoshi Nakadai, Takashi Onikubo, Mohamed Guermah, Daniela Rhodes, Robert G Roeder

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 42 citations in OpenAlex.

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  10. The A'-helix of CYP11A1 remodels mitochondrial cristae.Journal of biomedical science · 2022
    Article
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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

7 authors at 3 institutions in 3 countries.

Miho ShimadaLaboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY 10065, USA.
Wei-Yi ChenLaboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY 10065, USA; Institute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei 112, Taiwan; Cancer Progression Research Center, National Yang-Ming University, Taipei 112, Taiwan.
Tomoyoshi NakadaiLaboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY 10065, USA.
Takashi OnikuboLaboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY 10065, USA.
Mohamed GuermahLaboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY 10065, USA.
Daniela RhodesNTU Institute of Structural Biology and School of Biological Sciences, Nanyang Technological University, Singapore 636921, Singapore.
Robert G RoederLaboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY 10065, USA. Electronic address: roeder@rockefeller.edu.
Rockefeller University · USNanyang Technological University · SGNational Yang Ming Chiao Tung University · TW

Funding

Nuclear Receptor Coactivator Functions and MechanismsR01DK071900 · NIDDK · ROCKEFELLER UNIVERSITY · PI ROEDER, ROBERT G · 2005 to 2015
$5.9M
Mechanisms of p53 target gene activation in DNA damage responsesR01CA129325 · NCI · ROCKEFELLER UNIVERSITY · PI ROEDER, ROBERT G · 2007 to 2011
$4.0M
Transcriptional regulatory mechanisms in B cell development and leukemogenesisR01CA178765 · NCI · ROCKEFELLER UNIVERSITY · PI ROEDER, ROBERT G · 2013 to 2017
$2.8M
NCI NIH HHS R01 CA129325NCI NIH HHS R01 CA178765NIDDK NIH HHS R01 DK071900
6 · The paper itself

Abstract

Linker histone H1 has been correlated with transcriptional inhibition, but the mechanistic basis of the inhibition and its reversal during gene activation has remained enigmatic. We report that H1-compacted chromatin, reconstituted in vitro, blocks transcription by abrogating core histone modifications by p300 but not activator and p300 binding. Transcription from H1-bound chromatin is elicited by the H1 chaperone NAP1, which is recruited in a gene-specific manner through direct interactions with activator-bound p300 that facilitate core histone acetylation (by p300) and concomitant eviction of H1 and H2A-H2B. An analysis in B cells confirms the strong dependency on NAP1-mediated H1 eviction for induction of the silent CD40 gene and further demonstrates that H1 eviction, seeded by activator-p300-NAP1-H1 interactions, is propagated over a CCCTC-binding factor (CTCF)-demarcated region through a distinct mechanism that also involves NAP1. Our results confirm direct transcriptional inhibition by H1 and establish a gene-specific H1 eviction mechanism through an activator→p300→NAP1→H1 pathway.

Indexed as

Transcription, GeneticAcetylationBinding SitesB-LymphocytesCCCTC-Binding FactorCD40 AntigensChromatinE1A-Associated p300 ProteinHistone CodeHistonesHumansMolecular ChaperonesNucleosomesPromoter Regions, GeneticProtein BindingProteinsCCCTC-Binding FactorCD40 AntigensChromatinE1A-Associated p300 ProteinEP300 protein, humanHistonesMolecular ChaperonesNucleosomesProteinsTRMO protein, humantRNA MethyltransferasesB cell maturationCTCFhigher-order chromatinin vitro transcriptionlinker histoneNAP1NF-κBp300transcription

Identifiers

PMID30902546
PMCPMC6598686
OpenAlexW2923700619

What OpenQuestion holds

Textmetadata
LicenceTDM
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.