Evidence map›Paper›PMID 23393134›Full record

ArticleThe Journal of biological chemistry2013

The tumor suppressor kinase LKB1 activates the downstream kinases SIK2 and SIK3 to stimulate nuclear export of class IIa histone deacetylases.

Donald R Walkinshaw, Ryan Weist, Go-Woon Kim, Linya You, Lin Xiao, Jianyun Nie, Cathy S Li, Songping Zhao, Minghong Xu, Xiang-Jiao Yang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Gene model for the ortholog ofmicroPublication biology · 2025
    Article
  7. HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. SIK3-HDAC4 in the suprachiasmatic nucleus regulates the timing of arousal at the dark onset and circadian period in mice.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review

6 more citing papers are in PubMed but not listed here.

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 1 institution in 2 countries.

Donald R WalkinshawRosalind and Morris Goodman Cancer Research Center, McGill University, Montréal, Québec H3A 1A3, Canada.
Ryan Weist
Go-Woon Kim
Linya You
Lin Xiao
Jianyun Nie
Cathy S Li
Songping Zhao
Minghong Xu
Xiang-Jiao Yang
McGill University · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Histone deacetylases 4 (HDAC4), -5, -7, and -9 form class IIa within the HDAC superfamily and regulate diverse physiological and pathological cellular programs. With conserved motifs for phosphorylation-dependent 14-3-3 binding, these deacetylases serve as novel signal transducers that are able to modulate histone acetylation and gene expression in response to extracellular cues. Here, we report that in a PKA-sensitive manner the tumor suppressor kinase LKB1 acts through salt-inducible kinase 2 (SIK2) and SIK3 to promote nucleocytoplasmic trafficking of class IIa HDACs. Both SIK2 and SIK3 phosphorylate the deacetylases at the conserved motifs and stimulate 14-3-3 binding. SIK2 activates MEF2-dependent transcription and relieves repression of myogenesis by the deacetylases. Distinct from SIK2, SIK3 induces nuclear export of the deacetylases independent of kinase activity and 14-3-3 binding. These findings highlight the difference among members of the SIK family and indicate that LKB1-dependent SIK activation constitutes an important signaling module upstream from class IIa deacetylases for regulating cellular programs controlled by MEF2 and other transcription factors.

Indexed as

14-3-3 ProteinsAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesAnimalsCell Line, TumorCyclic AMP-Dependent Protein KinasesCytoplasmGenes, ReporterHEK293 CellsHeLa CellsHistone DeacetylasesHumansMiceProtein BindingProtein KinasesProtein Serine-Threonine Kinases14-3-3 ProteinsAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesCyclic AMP-Dependent Protein KinasesHistone DeacetylasesProtein KinasesProtein Serine-Threonine Kinasessalt-inducible kinase-2, humansalt-inducible kinase-2, mouseSIK3 protein, humanSIK3 protein, mouseSTK11 protein, humanStk11 protein, mouse

Identifiers

PMID23393134
PMCPMC3611005
OpenAlexW2052966638

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.