Evidence map›Paper›PMID 12629168›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003

Role of integrin-linked kinase in nerve growth factor-stimulated neurite outgrowth.

Julia Mills, Murat Digicaylioglu, Arthur T Legg, Clint E Young, Sean S Young, Alasdair M Barr, Lauren Fletcher, Timothy P O'Connor, Shoukat Dedhar

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Integrin-linked kinase (ILK): the known vs. the unknown and perspectives.Cellular and molecular life sciences : CMLS · 2022
    Review
  5. Article
  6. Article
  7. Article
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  9. Review
  10. Dysregulation of PINCH signaling in mesial temporal epilepsy.Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia · 2017
    Article
  11. Integrins in the Spotlight of Cancer.International journal of molecular sciences · 2016
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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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

9 authors at 3 institutions in 2 countries.

Julia MillsDepartment of Biochemistry and Molecular Biology, University of British Columbia, Vancouver, Canada V6T 123.
Murat Digicaylioglu
Arthur T Legg
Clint E Young
Sean S Young
Alasdair M Barr
Lauren Fletcher
Timothy P O'Connor
Shoukat Dedhar
University of British Columbia · CABC Cancer Agency · CASanford Burnham Prebys Medical Discovery Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of integrin-linked kinase (ILK), a kinase that is involved in various cellular processes, including adhesion and migration, has not been studied in primary neurons. Using mRNA dot blot and Western blot analysis of ILK in rat and human brain tissue, we found that ILK is expressed in various regions of the CNS. Immunohistochemical and immunocytochemical techniques revealed granular ILK staining that is enriched in neurons and colocalizes with the beta1 integrin subunit. The role of ILK in neurite growth promotion by NGF was studied in rat pheochromocytoma cells and dorsal root ganglion neurons using a pharmacological inhibitor of ILK (KP-392) or after overexpression of dominant-negative ILK (ILK-DN). Both molecular and pharmacological inhibition of ILK activity significantly reduced NGF-induced neurite outgrowth. Survival assays indicate that KP-392-induced suppression of neurite outgrowth occurred in the absence of cell death. ILK kinase activity was stimulated by NGF. NGF-mediated stimulation of phosphorylation of both AKT and the Tau kinase glycogen synthase kinase-3 (GSK-3) was inhibited in the presence of KP-392 and after overexpression of ILK-DN. Consequently, ILK inhibition resulted in an increase in the hyperphosphorylation of Tau, a substrate of GSK-3. Together these findings indicate that ILK is an important effector in NGF-mediated neurite outgrowth.

Indexed as

AnimalsCells, CulturedCell SurvivalCerebellumChick EmbryoEnzyme InhibitorsExtracellular MatrixGanglia, SpinalGlycogen Synthase Kinase 3HippocampusHumansImmunohistochemistryIntegrin beta1Nerve Growth FactorNeuritesNeuronsAKT1 protein, humanAkt1 protein, ratEnzyme InhibitorsGlycogen Synthase Kinase 3Integrin beta1Nerve Growth FactorProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRNA, MessengerScaffold Protein ILKtau Proteins

Identifiers

PMID12629168
PMCPMC6741947
OpenAlexW1897926848

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.