Evidence map›Paper›PMID 31106266›Full record

ArticleScience advances2019

PES1 is a critical component of telomerase assembly and regulates cellular senescence.

Long Cheng, Bin Yuan, Sunyang Ying, Chang Niu, Hongxu Mai, Xin Guan, Xiaohui Yang, Yan Teng, Jing Lin, Junjian Huang and 12 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. PES1 reduces CD8Journal of biomedical science · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

22 authors at 6 institutions in 1 country.

Long ChengDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing 100850, China.ORCID 0000-0002-4752-1298
Bin YuanDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing 100850, China.ORCID 0000-0001-8728-2263
Sunyang YingDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing 100850, China.ORCID 0000-0001-6185-6695
Chang NiuDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing 100850, China.ORCID 0000-0002-4512-917X
Hongxu MaiDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing 100850, China.
Xin GuanDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing 100850, China.
Xiaohui YangCAS Key Laboratory of Biomedical Diagnostics, Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, Suzhou 215163, China.ORCID 0000-0001-5175-5209
Yan TengState Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing 102206, China.
Jing LinFirst Affiliated Hospital, Chinese PLA General Hospital, Beijing 100048, China.ORCID 0000-0002-4654-9694
Junjian HuangDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing 100850, China.
Rui JinDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing 100850, China.
Jun WuDepartment of Microorganism Engineering, Beijing Institute of Biotechnology, Beijing 100071, China.
Bo LiuDepartment of Microorganism Engineering, Beijing Institute of Biotechnology, Beijing 100071, China.ORCID 0000-0001-6655-1866
Shaohong ChangDepartment of Microorganism Engineering, Beijing Institute of Biotechnology, Beijing 100071, China.
Enqun WangDepartment of Stomatology, Anqing Municipal Hospital of Anhui Medical University, Anqing, Anhui 246003, China.
Chunxia ZhangDepartment of Stomatology, Anqing Municipal Hospital of Anhui Medical University, Anqing, Anhui 246003, China.
Ning HouState Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing 102206, China.
Xuan ChengState Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing 102206, China.
Danyang XuDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing 100850, China.
Xiao YangState Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing 102206, China.ORCID 0000-0002-0298-9831
Shan GaoDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing 100850, China.ORCID 0000-0003-0262-4549
Qinong YeDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing 100850, China.ORCID 0000-0002-4654-9694
Peking University · CNBeijing Proteome Research Center · CNChinese Academy of Sciences · CNAnqing City Hospital · CNAnhui Medical University · CNFirst Affiliated Hospital of Chinese PLA General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Telomerase defers the onset of telomere shortening and cellular senescence by adding telomeric repeat DNA to chromosome ends, and its activation contributes to carcinogenesis. Telomerase minimally consists of the telomerase reverse transcriptase (TERT) and the telomerase RNA (TR). However, how telomerase assembles is largely unknown. Here, we demonstrate that PES1 (Pescadillo), a protein overexpressed in many cancers, forms a complex with TERT and TR through direct interaction with TERT, regulating telomerase activity, telomere length maintenance, and senescence. PES1 does not interact with the previously reported telomerase components Reptin, Pontin, p23, and Hsp90. PES1 facilitates telomerase assembly by promoting direct interaction between TERT and TR without affecting TERT and TR levels. PES1 expression correlates positively with telomerase activity and negatively with senescence in patients with breast cancer. Thus, we identify a previously unknown telomerase complex, and targeting PES1 may open a new avenue for cancer therapy.

Indexed as

Cellular SenescenceGene Expression Regulation, NeoplasticAnimalsApoptosisBreast NeoplasmsCell CycleCell Line, TumorDNA-Binding ProteinsFibroblastsGene Expression ProfilingHEK293 CellsHep G2 CellsHumansMCF-7 CellsMiceMice, KnockoutDNA-Binding ProteinsPES1 protein, humanPes1 protein, mouseRNA-Binding ProteinsRNA, Small InterferingTelomeraseTERT protein, humanTert protein, mouse

Identifiers

PMID31106266
PMCPMC6520020
OpenAlexW2944859905

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.