Evidence map›Paper›PMID 30118183›Full record

ReviewWiley interdisciplinary reviews. RNA2018

Glycogen synthase kinase-3 and alternative splicing.

Xiaolei Liu, Peter S Klein

Abstract readReview
In one paragraph

Review in Wiley interdisciplinary reviews. RNA, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. A mitochondrial surveillance mechanism activated bybioRxiv : the preprint server for biology · 2024
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Targeting the coronavirus nucleocapsid protein through GSK-3 inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Article
  15. Article
  16. Review
  17. Regulatory Functions ofFrontiers in physiology · 2020
    Article
  18. Article
  19. Review
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

2 authors at 1 institution in 1 country.

Xiaolei LiuDivision of Hematology-Oncology, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania.
Peter S KleinDivision of Hematology-Oncology, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania.
University of Pennsylvania · US

Funding

Maintenance and expansion of long-term hematopoietic stem cellsR01HL141759 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI KLEIN, PETER S · 2018 to 2021
$2.2M
Regulation of Neurogenesis and Behavior by GSK-3R01MH100923 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI KLEIN, PETER S · 2014 to 2017
$1.9M
An unexpected signaling output for the tumor suppressor APCR01GM115517 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI KLEIN, PETER S · 2016 to 2019
$1.3M
NHLBI NIH HHS R01 HL141759NIGMS NIH HHS R01 GM115517NIMH NIH HHS R01 MH100923
6 · The paper itself

Abstract

Glycogen synthase kinase-3 (GSK-3) is a highly conserved negative regulator of receptor tyrosine kinase, cytokine, and Wnt signaling pathways. Stimulation of these pathways inhibits GSK-3 to modulate diverse downstream effectors that include transcription factors, nutrient sensors, glycogen synthesis, mitochondrial function, circadian rhythm, and cell fate. GSK-3 also regulates alternative splicing in response to T-cell receptor activation, and recent phosphoproteomic studies have revealed that multiple splicing factors and regulators of RNA biosynthesis are phosphorylated in a GSK-3-dependent manner. Furthermore, inhibition of GSK-3 alters the splicing of hundreds of mRNAs, indicating a broad role for GSK-3 in the regulation of RNA processing. GSK-3-regulated phosphoproteins include SF3B1, SRSF2, PSF, RBM8A, nucleophosmin 1 (NPM1), and PHF6, many of which are mutated in leukemia and myelodysplasia. As GSK-3 is inhibited by pathways that are pathologically activated in leukemia and loss of Gsk3 in hematopoietic cells causes a severe myelodysplastic neoplasm in mice, these findings strongly implicate GSK-3 as a critical regulator of mRNA processing in normal and malignant hematopoiesis. This article is categorized under: RNA Processing > Splicing Mechanisms RNA Processing > Splicing Regulation/Alternative Splicing RNA in Disease and Development > RNA in Disease RNA Interactions with Proteins and Other Molecules > Protein-RNA Interactions: Functional Implications.

Indexed as

Alternative SplicingAnimalsGlycogen Synthase Kinase 3HumansMutationNeoplasmsNucleophosminGlycogen Synthase Kinase 3NPM1 protein, humanNpm1 protein, mouseNucleophosminglycogen synthase kinase-3leukemiamyelodysplasiasplicingWnt

Identifiers

PMID30118183
PMCPMC6185797
OpenAlexW2885202647

What OpenQuestion holds

Textmetadata
LicenceTDM
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.