Evidence map›Paper›PMID 25825522›Full record

ArticleMolecular and cellular biology2015

Serum- and Glucocorticoid-Inducible Kinase 1 Confers Protection in Cell-Based and in In Vivo Neurotoxin Models via the c-Jun N-Terminal Kinase Signaling Pathway.

Sarah Iqbal, Shannon Howard, Philip V LoGrasso

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Neurobiology of stress · 2023
    Review
  6. Article
  7. Article
  8. SGK1, autophagy and cancer: an overview.Molecular biology reports · 2022
    Review
  9. Review
  10. Convergent genomic and pharmacological evidence of PI3K/GSK3 signaling alterations in neurons from schizophrenia patients.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Genetic mutations you want.Proceedings of the National Academy of Sciences of the United States of America · 2016
    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 at 1 institution in 1 country.

Sarah IqbalDepartment of Molecular Therapeutics and Translational Research Institute, The Scripps Research Institute, Jupiter, Florida, USA.
Shannon HowardDepartment of Molecular Therapeutics and Translational Research Institute, The Scripps Research Institute, Jupiter, Florida, USA.
Philip V LoGrassoDepartment of Molecular Therapeutics and Translational Research Institute, The Scripps Research Institute, Jupiter, Florida, USA lograsso@scripps.edu.
Scripps Research Institute · US

Funding

Preclinical Development of JNK3 Inhibitors to Treat Parkinson's DiseaseU01NS057153 · NINDS · SCRIPPS RESEARCH INSTITUTE, THE · PI LOGRASSO, PHILIP · 2008 to 2012
$7.7M
Assay Development for Substrate and Phosphorylation State Specific JNK InhibitorsR01GM103825 · NIGMS · SCRIPPS FLORIDA · PI MCDONALD, PATRICIA HELEN · 2013 to 2015
$1.1M
NIGMS NIH HHS GM103825NIGMS NIH HHS R01 GM103825NINDS NIH HHS U01 NS057153NINDS NIH HHS U01-NS057153
6 · The paper itself

Abstract

Serum glucocorticoid kinase 1 (SGK1) has been shown to be protective in models of Parkinson's disease, but the details by which it confers benefit is unknown. The current study was designed to investigate the details by which SGK1 confers neuroprotection. To do this we employed a cellular neurodegeneration model to investigate c-Jun N-terminal kinase (JNK) signaling and endoplasmic reticulum (ER) stress induced by 6-hydroxydopamine. SGK1-expressing adenovirus was created and used to overexpress SGK1 in SH-SY5Y cells, and dexamethasone was used to increase endogenous expression of SGK1. Oxidative stress, mitochondrial dysfunction, and cell death were monitored to test the protective effect of SGK1. To investigate the effect of SGK1 overexpression in vivo, SGK1-expressing adenovirus was injected into the striatum of mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, and protection of dopaminergic neurons was quantitatively assessed by tyrosine hydroxylase immunohistochemistry. SGK1 overexpression was found to decrease reactive oxygen species generation, alleviate mitochondrial dysfunction, and rescue cell death in vitro and in vivo by inactivating mitogen-activated protein kinase kinase 4 (MKK4), JNK, and glycogen synthase kinase 3β (GSK3β) and thereby decreasing ER and oxidative stress. These results suggest that therapeutic strategies for activation of SGK1 may have the potential to be neuroprotective by deactivating the JNK and GSK3β pathways.

Indexed as

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAnimalsCell DeathCell Line, TumorDopaminergic NeuronsEndoplasmic ReticulumEndoplasmic Reticulum StressGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansImmediate-Early ProteinsJNK Mitogen-Activated Protein KinasesMaleMAP Kinase Kinase 4MiceMice, Inbred C57BL1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mouseImmediate-Early ProteinsJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 4Neuroprotective AgentsNeurotoxinsOxidopamineProtein Serine-Threonine KinasesReactive Oxygen SpeciesSerum-Glucocorticoid Regulated Kinases

Identifiers

PMID25825522
PMCPMC4420923
OpenAlexW1981579323

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.