Evidence map›Paper›PMID 28009085›Full record

ArticleStem cells (Dayton, Ohio)2017

Protein Tyrosine Phosphatase PRL2 Mediates Notch and Kit Signals in Early T Cell Progenitors.

Michihiro Kobayashi, Sarah C Nabinger, Yunpeng Bai, Momoko Yoshimoto, Rui Gao, Sisi Chen, Chonghua Yao, Yuanshu Dong, Lujuan Zhang, Sonia Rodriguez and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Targeting PRL phosphatases in hematological malignancies.Expert opinion on therapeutic targets · 2024
    Review
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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

19 authors at 6 institutions in 1 country.

Michihiro KobayashiDepartment of Pediatrics, Herman B Wells Center for Pediatric Research.
Sarah C NabingerDepartment of Pediatrics, Herman B Wells Center for Pediatric Research.
Yunpeng BaiDepartment of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Momoko YoshimotoDepartment of Pediatrics, Herman B Wells Center for Pediatric Research.
Rui GaoDepartment of Pediatrics, Herman B Wells Center for Pediatric Research.
Sisi ChenDepartment of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Chonghua YaoDepartment of Pediatrics, Herman B Wells Center for Pediatric Research.
Yuanshu DongDepartment of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Lujuan ZhangDepartment of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Sonia RodriguezDepartment of Pediatrics, Herman B Wells Center for Pediatric Research.
Yumi Yashiro-OhtaniDepartment of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
Warren S PearDepartment of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
Nadia CarlessoDepartment of Pediatrics, Herman B Wells Center for Pediatric Research.
Mervin C YoderDepartment of Pediatrics, Herman B Wells Center for Pediatric Research.
Reuben KapurDepartment of Pediatrics, Herman B Wells Center for Pediatric Research.
Mark H KaplanDepartment of Pediatrics, Herman B Wells Center for Pediatric Research.
Hugo Daniel LacorazzaDepartment of Pathology, Baylor College of Medicine, Texas Children's Hospital, Houston, Texas, USA.
Zhong-Yin ZhangDepartment of Medicinal Chemistry and Molecular Pharmacology, Purdue University, West Lafayette, Indiana, USA.
Yan LiuDepartment of Pediatrics, Herman B Wells Center for Pediatric Research.
Herman Miller (United States) · USIndiana University School of MedicineIndiana University – Purdue University Indianapolis · USUniversity of Pennsylvania · USPurdue University West Lafayette · USTexas Children's Hospital · US

Funding

Indiana Clinical and Translational Sciences InstituteUL1TR001108 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI DENNE, SCOTT C., SHEKHAR, ANANTHA · 2013 to 2017
$23.3M
Structure/Function of Protein Tyrosine PhosphatasesR01CA069202 · NCI · YESHIVA UNIVERSITY · PI Zhong-Yin Zhang · 1996 to 2026
$7.3M
Role of p21 activated kinase in LeukemogenesisR01CA173852 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPUR, REUBEN · 2014 to 2025
$3.4M
Physiologic Regulation of Hematopoiesis by NotchR01DK097837 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI CARLESSO, NADIA · 2014 to 2017
$1.6M
Targeting PRL2 phosphatase in acute myeloid leukemiaF32CA203049 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI NABINGER, SARAH C. · 2016 to 2017
$121k
NCATS NIH HHS UL1 TR001108NCI NIH HHS F32 CA203049NCI NIH HHS R01 CA069202NCI NIH HHS R01 CA173852NIDDK NIH HHS R01 DK097837
6 · The paper itself

Abstract

The molecular pathways regulating lymphoid priming, fate, and development of multipotent bone marrow hematopoietic stem and progenitor cells (HSPCs) that continuously feed thymic progenitors remain largely unknown. While Notch signal is indispensable for T cell specification and differentiation, the downstream effectors are not well understood. PRL2, a protein tyrosine phosphatase that regulates hematopoietic stem cell proliferation and self-renewal, is highly expressed in murine thymocyte progenitors. Here we demonstrate that protein tyrosine phosphatase PRL2 and receptor tyrosine kinase c-Kit are critical downstream targets and effectors of the canonical Notch/RBPJ pathway in early T cell progenitors. While PRL2 deficiency resulted in moderate defects of thymopoiesis in the steady state, de novo generation of T cells from Prl2 null hematopoietic stem cells was significantly reduced following transplantation. Prl2 null HSPCs also showed impaired T cell differentiation in vitro. We found that Notch/RBPJ signaling upregulated PRL2 as well as c-Kit expression in T cell progenitors. Further, PRL2 sustains Notch-mediated c-Kit expression and enhances stem cell factor/c-Kit signaling in T cell progenitors, promoting effective DN1-DN2 transition. Thus, we have identified a critical role for PRL2 phosphatase in mediating Notch and c-Kit signals in early T cell progenitors. Stem Cells 2017;35:1053-1064.

Indexed as

AnimalsAnimals, NewbornCell DifferentiationHematopoietic Stem CellsHematopoietic Stem Cell TransplantationImmediate-Early ProteinsImmunoglobulin J Recombination Signal Sequence-Binding ProteinMice, Inbred C57BLModels, BiologicalProtein Tyrosine PhosphatasesProto-Oncogene Proteins c-kitReceptors, NotchSignal TransductionStem CellsThymus GlandT-LymphocytesImmediate-Early ProteinsImmunoglobulin J Recombination Signal Sequence-Binding ProteinProtein Tyrosine PhosphatasesProto-Oncogene Proteins c-kitPtp4a2 protein, mouseRbpj protein, mouseReceptors, Notchc-KitEarly T lineage progenitorsNotchPRL2T cell progenitorsThymopoiesis

Identifiers

PMID28009085
PMCPMC5367971
OpenAlexW2566239759

What OpenQuestion holds

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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.