ArticleCell cycle (Georgetown, Tex.)2014
Fine-tuning the intensity of the PKB/Akt signal enables diverse physiological responses.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- PTGIS inhibited osteogenic and promoted angiogenic differentiation of bone marrow mesenchymal stem cells via endoplasmic reticulum stress mediated PI3K/AKT signaling.Stem cell research & therapy · 2026Article
- Role and mechanism of mesenchymal stem cells in endometrial receptivity remodeling.Frontiers in cell and developmental biology · 2026Review
- Modulation of the substrate specificity of the kinase PDK1 by distinct conformations of the full-length protein.Science signaling · 2023Article
- Article
- Reducing PDK1/Akt Activity: An Effective Therapeutic Target in the Treatment of Alzheimer's Disease.Cells · 2022Review
- Receptor-Mediated AKT/PI3K Signalling and Behavioural Alterations in Zebrafish Larvae Reveal Association between Schizophrenia and Opioid Use Disorder.International journal of molecular sciences · 2022Article
- Structural basis of Focal Adhesion Kinase activation on lipid membranes.The EMBO journal · 2020Article
- The Impact of the PI3K/Akt Signaling Pathway in Anxiety and Working Memory in Young and Middle-Aged PDK1 K465E Knock-In Mice.Frontiers in behavioral neuroscience · 2020Article
- Article
- Roles of PI3K/AKT/GSK3 Pathway Involved in Psychiatric Illnesses.Diseases (Basel, Switzerland) · 2019Review
- The miR-23a~27a~24-2 microRNA cluster buffers transcription and signaling pathways during hematopoiesis.PLoS genetics · 2017Article
- Reducing the Levels of Akt Activation by PDK1 Knock-in Mutation Protects Neuronal Cultures against Synthetic Amyloid-Beta Peptides.Frontiers in aging neuroscience · 2017Article
- Presynaptic Aβ40 prevents synapse addition in the adult Drosophila neuromuscular junction.PloS one · 2017Article
- Mutation of the 3-Phosphoinositide-Dependent Protein Kinase 1 (PDK1) Substrate-Docking Site in the Developing Brain Causes Microcephaly with Abnormal Brain Morphogenesis Independently of Akt, Leading to Impaired Cognition and Disruptive Behaviors.Molecular and cellular biology · 2016Article
- Alternative Activation Mechanisms of Protein Kinase B Trigger Distinct Downstream Signaling Responses.The Journal of biological chemistry · 2015Article
- Triple Akt inhibition as a new therapeutic strategy in T-cell acute lymphoblastic leukemia.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The PI3K/PDK1/PKB signaling pathway plays essential roles in regulating neuronal survival, differentiation and plasticity in response to neurotrophic factors, neurotransmitters and ion channels. Both PDK1 and PKB can interact at the plasma membrane with a phosphoinositide synthesized by PI3K, the second messenger PtdIns(3,4,5)P3, enabling PDK1 to phosphorylate and activate PKB. In the PDK1 K465E knock-in mice expressing a mutant form of PDK1 incapable of phosphoinositide binding, activation of PKB was markedly affected, but not totally abolished. It has been recently proposed that in the absence of PtdIns(3,4,5)P3 binding, PDK1 can still moderately activate PKB due to a docking site-mediated interaction of these 2 kinases. A recent report has uncovered that in the PDK1 K465E mice neurons, a PKB signal threshold was sufficient to support neuronal survival responses, whereas neuritogenesis, neuronal polarization and axon outgrowth were severely impaired. We propose here that the low-efficiency mechanism of PKB activation observed in the PDK1 K465E mice might represent the ancestral mechanism responsible for the essential functions of this pathway, while the phosphoinositide-dependent activation should be considered an evolutionary innovation that enabled the acquisition of novel functions.
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Registered trials
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.