Evidence map›Paper›PMID 28101375›Full record

ArticleCell discovery2017

Aurora-A promotes the establishment of spindle assembly checkpoint by priming the Haspin-Aurora-B feedback loop in late G2 phase.

Fazhi Yu, Ya Jiang, Lucy Lu, Mimi Cao, Yulong Qiao, Xing Liu, Dan Liu, Terry Van Dyke, Fangwei Wang, Xuebiao Yao and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell discovery, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Tumor-intrinsic CDC42BPB confers resistance to anti-PD-1 immune checkpoint blockade in breast cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  5. Haspin mediates H3.3S31 phosphorylation downstream of Aurora B in mouse embryonic stem cells.Protein science : a publication of the Protein Society · 2024
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. HASPIN kinase inhibitor CHR-6494 suppresses intestinal polyp development, cachexia, and hypogonadism in Apcmin/+ mice.European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) · 2020
    Article
  15. Article
  16. Review
  17. Article
  18. 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

12 authors at 6 institutions in 2 countries.

Fazhi YuKey Laboratory of Innate Immunity and Chronic Disease of CAS, Innovation Center for Cell Biology, School of Life Sciences, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China , Hefei, China.
Ya JiangKey Laboratory of Innate Immunity and Chronic Disease of CAS, Innovation Center for Cell Biology, School of Life Sciences, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China , Hefei, China.
Lucy LuCenter for Advanced Preclinical Research, the Center for Cancer Research, National Cancer Institute , Frederick, MD, USA.
Mimi CaoKey Laboratory of Innate Immunity and Chronic Disease of CAS, Innovation Center for Cell Biology, School of Life Sciences, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China , Hefei, China.
Yulong QiaoKey Laboratory of Innate Immunity and Chronic Disease of CAS, Innovation Center for Cell Biology, School of Life Sciences, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China , Hefei, China.
Xing LiuAnhui Key laboratory for Cellular Dynamics & Chemical Biology, Chinese Academy of Sciences Center for Excellence in Molecular Cell Science , Hefei, China.
Dan LiuKey Laboratory of Innate Immunity and Chronic Disease of CAS, Innovation Center for Cell Biology, School of Life Sciences, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China , Hefei, China.
Terry Van DykeCenter for Advanced Preclinical Research, the Center for Cancer Research, National Cancer Institute , Frederick, MD, USA.
Fangwei WangLife Sciences Institute and Innovation Center for Cell Biology, Zhejiang University , Hangzhou, China.
Xuebiao YaoAnhui Key laboratory for Cellular Dynamics & Chemical Biology, Chinese Academy of Sciences Center for Excellence in Molecular Cell Science , Hefei, China.
Jing GuoKey Laboratory of Innate Immunity and Chronic Disease of CAS, Innovation Center for Cell Biology, School of Life Sciences, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China , Hefei, China.
Zhenye YangKey Laboratory of Innate Immunity and Chronic Disease of CAS, Innovation Center for Cell Biology, School of Life Sciences, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China , Hefei, China.
Hefei National Center for Physical Sciences at Nanoscale · CNUniversity of Science and Technology of China · CNNational Cancer Institute · USCenter for Excellence in Molecular Cell Science · CNChinese Academy of Sciences · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aurora-A kinase functions mainly in centrosome maturation, separation and spindle formation. It has also been found to be amplified or overexpressed in a range of solid tumors, which is linked with tumor progression and poor prognosis. Importantly, Aurora-A inhibitors are being studied in a number of ongoing clinical trials. However, whether and how Aurora-A has a role in the regulation of the mitotic checkpoint is controversial. Additionally, the function of nuclear-accumulated Aurora-A in late G2 phase is not clear. Here we show that knockout, inhibition or blockade of the nuclear entry of Aurora-A severely decreased the centromere localization of Aurora-B and the phosphorylation of histone H3 threonine 3 (H3T3-ph) mediated by the kinase Haspin in late G2 phase. We further reveal that nuclear-accumulated Aurora-A phosphorylates Haspin at multiple sites at its N-terminus and that this promotes H3T3-ph and the rapid recruitment to the centromere of the chromosomal passenger complex. In addition, Aurora-A facilitates the association of Aurora-B with their common substrates: Haspin and Plk1. Notably, these functions of Aurora-A are mostly independent of Plk1. Thus we demonstrate that, in late G2 and prophase, Aurora-A phosphorylates Haspin to trigger the Haspin-H3T3-ph-Aurora-B positive feedback loop that supports the timely establishment of the chromosomal passenger complex and the mitotic checkpoint before spindle assembly.

Indexed as

Aurora-Achromosomal passenger complexH3T3-phHaspinspindle assembly checkpoint

Identifiers

PMID28101375
PMCPMC5223110
OpenAlexW2569442203

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.