Evidence map›Paper›PMID 25680095›Full record

ArticlePloS one2015

Ubiquitin specific protease 21 is dispensable for normal development, hematopoiesis and lymphocyte differentiation.

Jaspreet Pannu, Jad I Belle, Michael Förster, Claudia U Duerr, Shiyang Shen, Leanne Kane, Katherine Harcourt, Jörg H Fritz, Simon Clare, Anastasia Nijnik

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

28 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Ubiquitin-Dependent Regulation of Treg Function and Plasticity.Advances in experimental medicine and biology · 2021
    Article
  11. Journal of immunology research · 2021
    Article
  12. Article
  13. Review
  14. Deubiquitination and Stabilization of PD-L1 by USP21.American journal of translational research · 2021
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  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

10 authors at 2 institutions in 2 countries.

Jaspreet PannuDepartment of Physiology, McGill University, Montreal, Canada; Department of Biology, McGill University, Montreal, Canada.
Jad I BelleDepartment of Physiology, McGill University, Montreal, Canada; Complex Traits Group, McGill University, Montreal, Canada.
Michael FörsterDepartment of Physiology, McGill University, Montreal, Canada; Complex Traits Group, McGill University, Montreal, Canada.
Claudia U DuerrComplex Traits Group, McGill University, Montreal, Canada; Department of Microbiology and Immunology, McGill University, Montreal, Canada.
Shiyang ShenDepartment of Physiology, McGill University, Montreal, Canada; Complex Traits Group, McGill University, Montreal, Canada.
Leanne KaneWellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, United Kingdom.
Katherine HarcourtWellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, United Kingdom.
Jörg H FritzComplex Traits Group, McGill University, Montreal, Canada; Department of Microbiology and Immunology, McGill University, Montreal, Canada.
Simon ClareWellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, United Kingdom.
Anastasia NijnikDepartment of Physiology, McGill University, Montreal, Canada; Complex Traits Group, McGill University, Montreal, Canada.
McGill University · CAWellcome Sanger Institute · GB

Funding

CIHRWellcome TrustWellcome Trust 098051
6 · The paper itself

Abstract

USP21 is a ubiquitin specific protease that catalyzes protein deubiquitination, however the identification of its physiological substrates remains challenging. USP21 is known to deubiquitinate transcription factor GATA3 and death-domain kinase RIPK1 in vitro, however the in vivo settings where this regulation plays a biologically significant role remain unknown. In order to determine whether USP21 is an essential and non-redundant regulator of GATA3 or RIPK1 activity in vivo, we characterized Usp21-deficient mice, focusing on mouse viability and development, hematopoietic stem cell function, and lymphocyte differentiation. The Usp21-knockout mice were found to be viable and fertile, with no significant dysmorphology, in contrast to the GATA3 and RIPK1 knockout lines that exhibit embryonic or perinatal lethality. Loss of USP21 also had no effect on hematopoietic stem cell function, lymphocyte development, or the responses of antigen presenting cells to TLR and TNFR stimulation. GATA3 levels in hematopoietic stem cells or T lymphocytes remained unchanged. We observed that aged Usp21-knockout mice exhibited spontaneous T cell activation, however this was not linked to altered GATA3 levels in the affected cells. The contrast in the phenotype of the Usp21-knockout line with the previously characterized GATA3 and RIPK1 knockout mice strongly indicates that USP21 is redundant for the regulation of GATA3 and RIPK1 activity during mouse development, in hematopoietic stem cells, and in lymphocyte differentiation. The Usp21-deficient mouse line characterized in this study may serve as a useful tool for the future characterization of USP21 physiological functions.

Indexed as

AnimalsCell DifferentiationDendritic CellsGATA3 Transcription FactorGene OrderGene TargetingGenetic LociHematopoiesisHematopoietic Stem CellsImmunophenotypingLymphocyte ActivationLymphocytesMacrophagesMiceMice, KnockoutReceptors, Tumor Necrosis FactorGATA3 Transcription FactorReceptors, Tumor Necrosis FactorToll-Like ReceptorsUbiquitin ThiolesteraseUsp16 protein, mouse

Identifiers

PMID25680095
PMCPMC4332479
OpenAlexW1997739317

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.