Evidence map›Paper›PMID 23154402›Full record

ReviewCell adhesion & migration

Ste20-like kinase SLK, at the crossroads: a matter of life and death.

Khalid N Al-Zahrani, Kyla D Baron, Luc A Sabourin

Abstract readReview
In one paragraph

Review in Cell adhesion & migration. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Ste20-like Kinase Is Critical for Inhibitory Synapse Maintenance and Its Deficiency Confers a Developmental Dendritopathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Ste20-like kinase, SLK, a novel mediator of podocyte integrity.American journal of physiology. Renal physiology · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

3 authors.

Khalid N Al-ZahraniOttawa Hospital Research Institute, Cancer Therapeutics, Ottawa, ON Canada.
Kyla D Baron
Luc A Sabourin

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Reorganization of the cytoskeleton is necessary for apoptosis, proliferation, migration, development and tissue repair. However, it is well established that mutations or overexpression of key regulators contribute to the phenotype and progression of several pathologies such as cancer. For instance, c-src mutations and the overexpression of FAK have been implicated in the invasive and metastatic process, suggesting that components of the motility system may represent a new class of therapeutic targets. Over the last several years, we and others have established distinct roles for the Ste20-like kinase SLK, encompassing apoptosis, growth, motility and development. Here, we review the SLK field from its initial cloning to the most recent findings from our laboratory. We summarize the various roles of SLK and the biochemical mechanisms that regulate its activity. These various findings reveal very complex functions and pattern of regulation for SLK in development and cancer, making it a potential therapeutic target.

Indexed as

ApoptosisSignal TransductionAnimalsCell AdhesionCell Line, TumorCell MovementCytoskeletonEnzyme ActivationErb-b2 Receptor Tyrosine KinasesFocal Adhesion Kinase 1Gene Expression Regulation, DevelopmentalGene Expression Regulation, NeoplasticHippo KinasesHumansMiceMice, KnockoutERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesFocal Adhesion Kinase 1Hippo KinasesProtein Serine-Threonine KinasesPTK2 protein, humanSLK protein, human

Identifiers

PMID23154402
PMCPMC3544772

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.