Evidence map›Paper›PMID 38002281›Full record

ArticleBiomolecules2023

PKN1 Exerts Neurodegenerative Effects in an In Vitro Model of Cerebellar Hypoxic-Ischemic Encephalopathy via Inhibition of AKT/GSK3β Signaling.

Stephanie Zur Nedden, Motahareh Solina Safari, Friedrich Fresser, Klaus Faserl, Herbert Lindner, Bettina Sarg, Gottfried Baier, Gabriele Baier-Bitterlich

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

Article in Biomolecules, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 32% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Role of PKN1 in Retinal Cell Type Formation.International journal of molecular sciences · 2024
    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

8 authors at 1 institution in 1 country.

Stephanie Zur NeddenInstitute of Neurobiochemistry, CCB-Biocenter, Medical University of Innsbruck, 6020 Innsbruck, Austria.
Motahareh Solina SafariInstitute of Neurobiochemistry, CCB-Biocenter, Medical University of Innsbruck, 6020 Innsbruck, Austria.
Friedrich FresserInstitute for Cell Genetics, Medical University of Innsbruck, 6020 Innsbruck, Austria.
Klaus FaserlProtein Core Facility, Institute of Medical Biochemistry, CCB-Biocenter, Medical University of Innsbruck, 6020 Innsbruck, Austria.ORCID 0000-0003-1646-3256
Herbert LindnerProtein Core Facility, Institute of Medical Biochemistry, CCB-Biocenter, Medical University of Innsbruck, 6020 Innsbruck, Austria.ORCID 0000-0003-1262-9976
Bettina SargProtein Core Facility, Institute of Medical Biochemistry, CCB-Biocenter, Medical University of Innsbruck, 6020 Innsbruck, Austria.
Gottfried BaierInstitute for Cell Genetics, Medical University of Innsbruck, 6020 Innsbruck, Austria.ORCID 0000-0002-2085-8325
Gabriele Baier-BitterlichInstitute of Neurobiochemistry, CCB-Biocenter, Medical University of Innsbruck, 6020 Innsbruck, Austria.
Innsbruck Medical University · AT

Funding

Austrian Science Fund FWF P 31085Austrian Science Fund FWF T 1091FWF Austrian Science Fund T1091 (to S.zN.); P31085-B26 (to G.B.-B.); P31383-B30 (to G.B.)
6 · The paper itself

Abstract

We recently identified protein kinase N1 (PKN1) as a negative gatekeeper of neuronal AKT protein kinase activity during postnatal cerebellar development. The developing cerebellum is specifically vulnerable to hypoxia-ischemia (HI), as it occurs during hypoxic-ischemic encephalopathy, a condition typically caused by oxygen deprivation during or shortly after birth. In that context, activation of the AKT cell survival pathway has emerged as a promising new target for neuroprotective interventions. Here, we investigated the role of PKN1 in an in vitro model of HI, using postnatal cerebellar granule cells (Cgc) derived from

Indexed as

Hypoxia-Ischemia, BrainNeuroprotective AgentsAnimalsAnimals, NewbornCerebellumGlycogen Synthase Kinase 3 betaHypoxiaMiceProtein Kinase CProto-Oncogene Proteins c-aktGlycogen Synthase Kinase 3 betaNeuroprotective AgentsProtein Kinase Cprotein kinase NProto-Oncogene Proteins c-aktAKTcerebellumhypoxic–ischemic encephalopathyprotein kinase N1

Identifiers

PMID38002281
PMCPMC10669522
OpenAlexW4388087780

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.