Evidence map›Paper›PMID 26822034›Full record

ArticleNature communications2016

Inactivation of nuclear GSK3β by Ser(389) phosphorylation promotes lymphocyte fitness during DNA double-strand break response.

Tina M Thornton, Pilar Delgado, Liang Chen, Beatriz Salas, Dimitry Krementsov, Miriam Fernandez, Santiago Vernia, Roger J Davis, Ruth Heimann, Cory Teuscher and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. Inactivation of GSK3β by SerCell death and differentiation · 2025
    Article
  4. Article
  5. The DNA repair kinase ATM regulates CD13 expression and cell migration.Frontiers in cell and developmental biology · 2024
    Article
  6. GSK3β Inhibition by Phosphorylation at SerInternational journal of molecular sciences · 2022
    Article
  7. Article
  8. Frontiers in genetics · 2022
    Article
  9. Article
  10. Review
  11. Regulation of GSK3β by SerMolecular neurobiology · 2021
    Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Failure to Inactivate Nuclear GSK3β by SerNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    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

13 authors at 5 institutions in 2 countries.

Tina M ThorntonDepartment of Medicine/Immunobiology, University of Vermont, Burlington, Vermont 05405, USA.
Pilar DelgadoB Cell Biology Lab, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid 328029, Spain.
Liang ChenDepartment of Immunology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Beatriz SalasDepartment of Medicine/Immunobiology, University of Vermont, Burlington, Vermont 05405, USA.
Dimitry KrementsovDepartment of Medicine/Immunobiology, University of Vermont, Burlington, Vermont 05405, USA.
Miriam FernandezDepartment of Medicine/Immunobiology, University of Vermont, Burlington, Vermont 05405, USA.
Santiago VerniaProgram in Molecular Medicine, University of Massachusetts, Worcester, Massachusetts 01605, USA.
Roger J DavisProgram in Molecular Medicine, University of Massachusetts, Worcester, Massachusetts 01605, USA.
Ruth HeimannDepartment of Medicine/Radiology, University of Vermont, Burlington, Vermont 05405, USA.
Cory TeuscherDepartment of Medicine/Immunobiology, University of Vermont, Burlington, Vermont 05405, USA.
Michael S KrangelDepartment of Immunology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Almudena R RamiroB Cell Biology Lab, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid 328029, Spain.
Mercedes RincónDepartment of Medicine/Immunobiology, University of Vermont, Burlington, Vermont 05405, USA.
University of Vermont · USDuke Medical Center · USSpanish National Centre for Cardiovascular Research · ESHoward Hughes Medical Institute · USUniversity of Massachusetts Chan Medical School · US

Funding

Vermont Immunobioloigy/ Infectious Diseases CenterP20GM103496 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BUDD, RALPH C · 2012 to 2015
$8.7M
Control Of Tcr Delta And Tcr Alpha RearrangementR37GM041052 · NIGMS · DUKE UNIVERSITY · PI KRANGEL, MICHAEL S · 2006 to 2015
$5.1M
P53 and cell cycle checkpoint by p38 MAP kinaseR01AI051454 · NIAID · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI RINCON, MERCEDES · 2003 to 2019
$4.9M
HUMAN GAMMA DELTA T CELL RECEPTORR01GM041052 · NIGMS · DUKE UNIVERSITY · PI KRANGEL, MICHAEL S · 1989 to 2019
$4.8M
Upgrade of a FACS Aria Cell SorterS10OD018175 · OD · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BOYSON, JONATHAN E · 2015 to 2015
$153k
Howard Hughes Medical InstituteNIAID NIH HHS R01 AI051454NIGMS NIH HHS P20 GM103496NIGMS NIH HHS R01 GM041052NIGMS NIH HHS R37 GM041052NIGMS NIH HHS R37 GM41052NIH HHS S10 OD018175
6 · The paper itself

Abstract

Variable, diversity and joining (V(D)J) recombination and immunoglobulin class switch recombination (CSR) are key processes in adaptive immune responses that naturally generate DNA double-strand breaks (DSBs) and trigger a DNA repair response. It is unclear whether this response is associated with distinct survival signals that protect T and B cells. Glycogen synthase kinase 3β (GSK3β) is a constitutively active kinase known to promote cell death. Here we show that phosphorylation of GSK3β on Ser(389) by p38 MAPK (mitogen-activated protein kinase) is induced selectively by DSBs through ATM (ataxia telangiectasia mutated) as a unique mechanism to attenuate the activity of nuclear GSK3β and promote survival of cells undergoing DSBs. Inability to inactivate GSK3β through Ser(389) phosphorylation in Ser(389)Ala knockin mice causes a decrease in the fitness of cells undergoing V(D)J recombination and CSR. Preselection-Tcrβ repertoire is impaired and antigen-specific IgG antibody responses following immunization are blunted in Ser(389)GSK3β knockin mice. Thus, GSK3β emerges as an important modulator of the adaptive immune response.

Indexed as

DNA Breaks, Double-StrandedAnimalsCells, CulturedDNA RepairGene Expression Regulation, EnzymologicGene Knock-In TechniquesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansLymphocytesMiceMutationPhosphorylationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mouse

Identifiers

PMID26822034
PMCPMC4740185
OpenAlexW2291227478

What OpenQuestion holds

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Registered trials

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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.