Evidence map›Paper›PMID 24371141›Full record

ArticleThe Journal of biological chemistry2014

Phosphatase of regenerating liver 2 (PRL2) deficiency impairs Kit signaling and spermatogenesis.

Yuanshu Dong, Lujuan Zhang, Yunpeng Bai, Hong-Ming Zhou, Amanda M Campbell, Hanying Chen, Weidong Yong, Wenjun Zhang, Qi Zeng, Weinian Shou and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.2field-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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Targeting PRL phosphatases in hematological malignancies.Expert opinion on therapeutic targets · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. International journal of molecular sciences · 2023
    Article
  9. Article
  10. Mechanism of PRL2 phosphatase-mediated PTEN degradation and tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

11 authors at 3 institutions in 2 countries.

Yuanshu DongFrom the Department of Biochemistry and Molecular Biology, and.
Lujuan Zhang
Yunpeng Bai
Hong-Ming Zhou
Amanda M Campbell
Hanying Chen
Weidong Yong
Wenjun Zhang
Qi Zeng
Weinian Shou
Zhong-Yin Zhang
Indiana University – Purdue University Indianapolis · USIndiana University School of MedicineAgency for Science, Technology and Research · SG

Funding

REGULATION OF CARDIOMYOCYTE SURVIVALP01HL085098 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI FIELD, LOREN J · 2007 to 2011
$10.9M
Structure/Function of Protein Tyrosine PhosphatasesR01CA069202 · NCI · YESHIVA UNIVERSITY · PI Zhong-Yin Zhang · 1996 to 2026
$7.3M
Role of LHX3 Protein Isoforms in Pituitary DevelopmentR01HD042024 · NICHD · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI RHODES, SIMON JAMES · 2002 to 2012
$2.6M
NCI NIH HHS R01 CA069202NHLBI NIH HHS P01 HL085098NICHD NIH HHS R01 HD042024
6 · The paper itself

Abstract

The Phosphatase of Regenerating Liver (PRL) proteins promote cell signaling and are oncogenic when overexpressed. However, our understanding of PRL function came primarily from studies with cultured cell lines aberrantly or ectopically expressing PRLs. To define the physiological roles of the PRLs, we generated PRL2 knock-out mice to study the effects of PRL deletion in a genetically controlled, organismal model. PRL2-deficient male mice exhibit testicular hypotrophy and impaired spermatogenesis, leading to decreased reproductive capacity. Mechanistically, PRL2 deficiency results in elevated PTEN level in the testis, which attenuates the Kit-PI3K-Akt pathway, resulting in increased germ cell apoptosis. Conversely, increased PRL2 expression in GC-1 cells reduces PTEN level and promotes Akt activation. Our analyses of PRL2-deficient animals suggest that PRL2 is required for spermatogenesis during testis development. The study also reveals that PRL2 promotes Kit-mediated PI3K/Akt signaling by reducing the level of PTEN that normally antagonizes the pathway. Given the strong cancer susceptibility to subtle variations in PTEN level, the ability of PRL2 to repress PTEN expression qualifies it as an oncogene and a novel target for developing anti-cancer agents.

Indexed as

AnimalsApoptosisFemaleGerm CellsImmediate-Early ProteinsMaleMiceMice, KnockoutPhosphatidylinositol 3-KinasesProtein Tyrosine PhosphatasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-kitPTEN PhosphohydrolaseSignal TransductionSpermatogenesisTestisImmediate-Early ProteinsPhosphatidylinositol 3-KinasesProtein Tyrosine PhosphatasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-kitPTEN PhosphohydrolasePten protein, mousePtp4a2 protein, mouseProtein PhosphatasePtenSignal TransductionSpermatogenesisTestis

Identifiers

PMID24371141
PMCPMC3916576
OpenAlexW2025068493

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.