Evidence map›Paper›PMID 29138236›Full record

ArticleEMBO reports2018

A kinase-dependent role for Haspin in antagonizing Wapl and protecting mitotic centromere cohesion.

Cai Liang, Qinfu Chen, Qi Yi, Miao Zhang, Haiyan Yan, Bo Zhang, Linli Zhou, Zhenlei Zhang, Feifei Qi, Sheng Ye and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EMBO reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 55 citations in OpenAlex.

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  17. Design of new disubstituted imidazo[1,2-Journal of enzyme inhibition and medicinal chemistry · 2020
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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

11 authors at 1 institution in 1 country.

Cai LiangLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Qinfu ChenLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Qi YiLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Miao ZhangLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Haiyan YanLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Bo ZhangLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Linli ZhouLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Zhenlei ZhangLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Feifei QiLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Sheng YeLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Fangwei WangLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China fwwang@zju.edu.cn.ORCID 0000-0001-5617-282X
Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sister-chromatid cohesion mediated by the cohesin complex is fundamental for precise chromosome segregation in mitosis. Through binding the cohesin subunit Pds5, Wapl releases the bulk of cohesin from chromosome arms in prophase, whereas centromeric cohesin is protected from Wapl until anaphase onset. Strong centromere cohesion requires centromeric localization of the mitotic histone kinase Haspin, which is dependent on the interaction of its non-catalytic N-terminus with Pds5B. It remains unclear how Haspin fully blocks the Wapl-Pds5B interaction at centromeres. Here, we show that the C-terminal kinase domain of Haspin (Haspin-KD) binds and phosphorylates the YSR motif of Wapl (Wapl-YSR), thereby directly inhibiting the YSR motif-dependent interaction of Wapl with Pds5B. Cells expressing a Wapl-binding-deficient mutant of Haspin or treated with Haspin inhibitors show centromeric cohesion defects. Phospho-mimetic mutation in Wapl-YSR prevents Wapl from binding Pds5B and releasing cohesin. Forced targeting Haspin-KD to centromeres partly bypasses the need for Haspin-Pds5B interaction in cohesion protection. Taken together, these results indicate a kinase-dependent role for Haspin in antagonizing Wapl and protecting centromeric cohesion in mitosis.

Indexed as

Chromosome SegregationAmino Acid MotifsAnaphaseCarrier ProteinsCell Cycle ProteinsCentromereChromatidsChromosomal Proteins, Non-HistoneCohesinsDNA-Binding ProteinsHeLa CellsHumansIntracellular Signaling Peptides and ProteinsMutationNuclear ProteinsPhosphorylationCarrier ProteinsCell Cycle ProteinsChromosomal Proteins, Non-HistoneCohesinsDNA-Binding ProteinsHASPIN protein, humanIntracellular Signaling Peptides and ProteinsNuclear ProteinsPDS5B protein, humanProtein Serine-Threonine KinasesProto-Oncogene ProteinsTranscription FactorsWAPL protein, humancohesinHaspinPds5Bsister‐chromatid cohesionWapl

Identifiers

PMID29138236
PMCPMC5757254
OpenAlexW2768594301

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.