Evidence map›Paper›PMID 27753532›Full record

ArticleCell cycle (Georgetown, Tex.)2016

Histone chaperone ASF1B promotes human β-cell proliferation via recruitment of histone H3.3.

Pradyut K Paul, Mary E Rabaglia, Chen-Yu Wang, Donald S Stapleton, Ning Leng, Christina Kendziorski, Peter W Lewis, Mark P Keller, Alan D Attie

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
1.2field-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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  8. The interaction betweenAnnals of medicine · 2023
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  14. Islet allografts expressing a PD-L1 and IDO fusion protein evade immune rejection and reverse preexisting diabetes in immunocompetent mice without systemic immunosuppression.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Pradyut K Paula Department of Biochemistry , University of Wisconsin , Madison , WI , USA.
Mary E Rabagliaa Department of Biochemistry , University of Wisconsin , Madison , WI , USA.
Chen-Yu Wanga Department of Biochemistry , University of Wisconsin , Madison , WI , USA.
Donald S Stapletona Department of Biochemistry , University of Wisconsin , Madison , WI , USA.
Ning Lengb Department of Statistics , University of Wisconsin , Madison , WI , USA.
Christina Kendziorskic Department of Biostatistics and Medical Informatics , University of Wisconsin , Madison , WI , USA.
Peter W Lewisd Department of Biomolecular Chemistry , University of Wisconsin , Madison , WI , USA.
Mark P Kellera Department of Biochemistry , University of Wisconsin , Madison , WI , USA.
Alan D Attiea Department of Biochemistry , University of Wisconsin , Madison , WI , USA.
University of Wisconsin–Madison · US

Funding

Shared Resources Core 2: Quantitative Proteomics CoreP01CA196539 · NCI · ROCKEFELLER UNIVERSITY · PI MUIR, TOM · 2015 to 2024
$17.6M
NCI NIH HHS P01 CA196539
6 · The paper itself

Abstract

Anti-silencing function 1 (ASF1) is a histone H3-H4 chaperone involved in DNA replication and repair, and transcriptional regulation. Here, we identify ASF1B, the mammalian paralog to ASF1, as a proliferation-inducing histone chaperone in human β-cells. Overexpression of ASF1B led to distinct transcriptional signatures consistent with increased cellular proliferation and reduced cellular death. Using multiple methods of monitoring proliferation and mitotic progression, we show that overexpression of ASF1B is sufficient to induce human β-cell proliferation. Co-expression of histone H3.3 further augmented β-cell proliferation, whereas suppression of endogenous H3.3 attenuated the stimulatory effect of ASF1B. Using the histone binding-deficient mutant of ASF1B (V94R), we show that histone binding to ASF1B is required for the induction of β-cell proliferation. In contrast to H3.3, overexpression of histone H3 variants H3.1 and H3.2 did not have an impact on ASF1B-mediated induction of proliferation. Our findings reveal a novel role of ASF1B in human β-cell replication and show that ASF1B and histone H3.3A synergistically stimulate human β-cell proliferation.

Indexed as

AnimalsApoptosisCell Cycle ProteinsCell LineCell ProliferationDNA DamageGene Expression RegulationHistone ChaperonesHistonesHumansInsulin-Secreting CellsMice, Inbred C57BLMitosisProtein BindingTranscription, GeneticASF1B protein, humanCell Cycle ProteinsHistone ChaperonesHistonesASF1Bcell cyclehistone H3.3replication-independent histone depositionβ-cell proliferation

Identifiers

PMID27753532
PMCPMC5176155
OpenAlexW2533095644

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.