Evidence map›Paper›PMID 26012568›Full record

ArticleBlood2015

Phosphatase Wip1 controls antigen-independent B-cell development in a p53-dependent manner.

Weiwei Yi, Xuelian Hu, Zhiyang Chen, Leiming Liu, Yuan Tian, Hui Chen, Yu-Sheng Cong, Fan Yang, Lianfeng Zhang, Karl Lenhard Rudolph and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. WIP1 phosphatase as pharmacological target in cancer therapy.Journal of molecular medicine (Berlin, Germany) · 2017
    Review
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 3 countries.

Weiwei YiInstitute of Aging Research, Hangzhou Normal University School of Medicine, Hangzhou, China;
Xuelian HuTransplantation Biology Research Division, State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China;
Zhiyang ChenInstitute of Aging Research, Hangzhou Normal University School of Medicine, Hangzhou, China; Leibniz Institute for Age Research-Fritz Lipmann Institute, Jena, Germany;
Leiming LiuInstitute of Aging Research, Hangzhou Normal University School of Medicine, Hangzhou, China; Sir Runrun Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China;
Yuan TianTransplantation Biology Research Division, State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China;
Hui ChenTransplantation Biology Research Division, State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China;
Yu-Sheng CongInstitute of Aging Research, Hangzhou Normal University School of Medicine, Hangzhou, China;
Fan YangTransplantation Biology Research Division, State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China;
Lianfeng ZhangKey Laboratory of Human Diseases Comparative Medicine, Ministry of Health; Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; and.
Karl Lenhard RudolphLeibniz Institute for Age Research-Fritz Lipmann Institute, Jena, Germany;
Zhixin ZhangDepartment of Pediatrics, West China Second University Hospital, State Key Laboratory of Biotherapy, Ministry of Education Key Laboratory of Birth Defects, Sichuan University, Chengdu, China.
Yong ZhaoTransplantation Biology Research Division, State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China;
Zhenyu JuInstitute of Aging Research, Hangzhou Normal University School of Medicine, Hangzhou, China;
Hangzhou Normal University · CNInstitute of Zoology · CNInstitute of Laboratory Animal Science · CNLeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DEState Key Laboratory of Biotherapy

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wild-type p53-induced phosphatase 1 (Wip1), a phosphatase previously considered as an oncogene, has been implicated in the regulation of thymus homeostasis and neutrophil maturation. However, the role of Wip1 in B-cell development is unknown. We show that Wip1-deficient mice exhibit a significant reduction of B-cell numbers in the bone marrow, peripheral blood, and spleen. A reciprocal transplantation approach revealed a cell-intrinsic defect in early B-cell precursors caused by Wip1 deficiency. Further experiments revealed that Wip1 deficiency led to a sustained activation of p53 in B cells, which led to increased level of apoptosis in the pre-B-cell compartment. Notably, the impairment of B-cell development in Wip1-deficient mice was completely rescued by genetic ablation of p53, but not p21. Therefore, loss of Wip1 phosphatase induces a p53-dependent, but p21-independent, mechanism that impairs B-cell development by enhancing apoptosis in early B-cell precursors. Moreover, Wip1 deficiency exacerbated a decline in B-cell development caused by aging as evidenced in mice with aging and mouse models with serial competitive bone marrow transplantation, respectively. Our present data indicate that Wip1 plays a critical role in maintaining antigen-independent B-cell development in the bone marrow and preventing an aging-related decline in B-cell development.

Indexed as

AgingAnimalsApoptosisB-LymphocytesBone Marrow CellsCell DifferentiationCyclin-Dependent Kinase Inhibitor p21FemaleLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutPhosphoprotein PhosphatasesPrecursor Cells, B-LymphoidProtein Phosphatase 2CSignal TransductionCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21Phosphoprotein PhosphatasesPPM1D protein, humanPpm1d protein, mouseProtein Phosphatase 2CTumor Suppressor Protein p53

Identifiers

PMID26012568
PMCPMC4520877
OpenAlexW1621837727

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.