Evidence map›Paper›PMID 37607329›Full record

ReviewFEBS letters2023

Functions of SRPK, CLK and DYRK kinases in stem cells, development, and human developmental disorders.

Elizabeth K J Hogg, Greg M Findlay

Open access · hybridAbstract readReview
In one paragraph

Review in FEBS letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. RNA Splicing as a Therapeutic Target in Cancer.Annual review of pharmacology and toxicology · 2026
    Review
  6. Article
  7. Review
  8. SR Protein Kinase is expressed inmicroPublication biology · 2025
    Article
  9. Article
  10. 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

2 authors at 1 institution in 1 country.

Elizabeth K J HoggThe MRC Protein Phosphorylation and Ubiquitylation Unit, School of Life Sciences, University of Dundee, UK.ORCID 0000-0002-2509-3202
Greg M FindlayThe MRC Protein Phosphorylation and Ubiquitylation Unit, School of Life Sciences, University of Dundee, UK.ORCID 0000-0002-7222-4965
University of Dundee · GB

Funding

Wellcome TrustWellcome Trust 211209/Z/18/Z
6 · The paper itself

Abstract

Human developmental disorders encompass a wide range of debilitating physical conditions and intellectual disabilities. Perturbation of protein kinase signalling underlies the development of some of these disorders. For example, disrupted SRPK signalling is associated with intellectual disabilities, and the gene dosage of DYRKs can dictate the pathology of disorders including Down's syndrome. Here, we review the emerging roles of the CMGC kinase families SRPK, CLK, DYRK, and sub-family HIPK during embryonic development and in developmental disorders. In particular, SRPK, CLK, and DYRK kinase families have key roles in developmental signalling and stem cell regulation, and can co-ordinate neuronal development and function. Genetic studies in model organisms reveal critical phenotypes including embryonic lethality, sterility, musculoskeletal errors, and most notably, altered neurological behaviours arising from defects of the neuroectoderm and altered neuronal signalling. Further unpicking the mechanisms of specific kinases using human stem cell models of neuronal differentiation and function will improve our understanding of human developmental disorders and may provide avenues for therapeutic strategies.

Indexed as

Dyrk KinasesIntellectual DisabilityProtein Serine-Threonine KinasesChildDevelopmental DisabilitiesHumansPhosphorylationProtein-Tyrosine KinasesStem CellsClk dual-specificity kinasesDYRK1A protein, humanDyrk KinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesCLKdifferentiationDYRKembryonic developmentHIPKintellectual disabilitykinase signallingneurodevelopmentphosphorylationSRPKstem cells

Identifiers

PMID37607329
PMCPMC10952393
OpenAlexW4386054828

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.