Evidence map›Paper›PMID 27744293›Full record

ArticleBiology open2016

Regulation of DNA replication and chromosomal polyploidy by the MLL-WDR5-RBBP5 methyltransferases.

Fei Lu, Xiaojun Wu, Feng Yin, Christina Chia-Fang Lee, Min Yu, Ivailo S Mihaylov, Jiekai Yu, Hong Sun, Hui Zhang

Open access · goldAbstract read
In one paragraph

Article in Biology open, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

7 citing papers in PubMed, 15 citations in OpenAlex.

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  7. KDM5B demethylates H3K4 to recruit XRCC1 and promote chemoresistance.International journal of biological sciences · 2018
    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

9 authors at 2 institutions in 2 countries.

Fei LuLaboratory of Chemical Genomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen, Guangdong 518055, China Basic Science Division, Nevada Cancer Institute, Las Vegas, NV 89135, USA.
Xiaojun WuLaboratory of Chemical Genomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen, Guangdong 518055, China.
Feng YinLaboratory of Chemical Genomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen, Guangdong 518055, China.
Christina Chia-Fang LeeBasic Science Division, Nevada Cancer Institute, Las Vegas, NV 89135, USA.
Min YuLaboratory of Chemical Genomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen, Guangdong 518055, China.
Ivailo S MihaylovBasic Science Division, Nevada Cancer Institute, Las Vegas, NV 89135, USA.
Jiekai YuDepartment of Chemistry and Biochemistry, University of Nevada, Las Vegas, NV 89154, USA.
Hong SunBasic Science Division, Nevada Cancer Institute, Las Vegas, NV 89135, USA Department of Chemistry and Biochemistry, University of Nevada, Las Vegas, NV 89154, USA.
Hui ZhangBasic Science Division, Nevada Cancer Institute, Las Vegas, NV 89135, USA Department of Chemistry and Biochemistry, University of Nevada, Las Vegas, NV 89154, USA hui.zhang@unlv.edu.ORCID http://orcid.org/0000-0001-6028-2554
Peking University · CNUniversity of Nevada, Las Vegas · US

Funding

Control of Epigenetic Inheritance By ProteolysisR15GM116087 · NIGMS · UNIVERSITY OF NEVADA LAS VEGAS · PI ZHANG, HUI · 2015 to 2015
$362k
NIGMS NIH HHS R15 GM116087
6 · The paper itself

Abstract

DNA replication licensing occurs on chromatin, but how the chromatin template is regulated for replication remains mostly unclear. Here, we have analyzed the requirement of histone methyltransferases for a specific type of replication: the DNA re-replication induced by the downregulation of either Geminin, an inhibitor of replication licensing protein CDT1, or the CRL4CDT2 ubiquitin E3 ligase. We found that siRNA-mediated reduction of essential components of the MLL-WDR5-RBBP5 methyltransferase complexes including WDR5 or RBBP5, which transfer methyl groups to histone H3 at K4 (H3K4), suppressed DNA re-replication and chromosomal polyploidy. Reduction of WDR5/RBBP5 also prevented the activation of H2AX checkpoint caused by re-replication, but not by ultraviolet or X-ray irradiation; and the components of MLL complexes co-localized with the origin recognition complex (ORC) and MCM2-7 replicative helicase complexes at replication origins to control the levels of methylated H3K4. Downregulation of WDR5 or RBBP5 reduced the methylated H3K4 and suppressed the recruitment of MCM2-7 complexes onto replication origins. Our studies indicate that the MLL complexes and H3K4 methylation are required for DNA replication but not for DNA damage repair.

Indexed as

DNA replicationH3K4 methylationRBBP5Re-replicationWDR5

Identifiers

PMID27744293
PMCPMC5087680
OpenAlexW2534422312

What OpenQuestion holds

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LicenceCC BY
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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.