Insulin-Like Growth Factor 1 Inhibits Extracellular Signal-Regulated Kinase to Promote Neuronal Survival via the Phosphatidylinositol 3-Kinase/Protein Kinase A/c-Raf Pathway

Subramaniam, Srinivasa; Shahani, Neelam; Strelau, Jens; Laliberté, Christine; Brandt, Roland; Kaplan, David R.; Unsicker, Klaus

doi:10.1523/jneurosci.5060-04.2005

Cited by 85 publications

(59 citation statements)

References 76 publications

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“…The specificity of LY-2949002 on PI3-K activity was further confirmed by the lack of rescue effect observed with IGF-I, a growth factor that predominantly signals through PI3-K in granule neurons (Fig. 4) (D 0 Mello et al 1997;Yamagashi et al 2003;Subramaniam et al 2005).…”

Section: Bzatp Protects Granule Neurons From Apoptosis Induced By Pi3mentioning

confidence: 76%

P2X7 Nucleotide Receptor is Coupled to GSK-3 Inhibition and Neuroprotection in Cerebellar Granule Neurons

et al. 2009

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In this study we report the coupling of nucleotide receptors to GSK-3 signalling, a relevant survival pathway in cerebellar granule neurons. P2X 7 agonist BzATP induced a 3-4-fold increase in GSK-3 phosphorylation, which is reported to be associated with the catalytic activity inhibition. This effect was dependent on extracellular calcium and PKC, and independent of PI3-K (phosphatidyl-inositol-3-kinase)/Akt, the main survival route of neurotrophins. BzATP also prevented the apoptosis of granule neurons induced by the pharmacological inhibition of the PI3-K signalling. Both effects, BzATPmediated GSK-3 phosphorylation and neuroprotection, were abolished by P2X 7 receptor antagonists, BBG, PPADS and A-438079. We found that BzATP prevented the progressive GSK-3 dephosphorylation and caspase-3 activation occurring under conditions of sustained PI3-K inhibition. These results reveal that P2X 7 receptor activation could provide a relevant survival route alternative to classical neurotrophic factors.

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Section: Bzatp Protects Granule Neurons From Apoptosis Induced By Pi3mentioning

confidence: 76%

P2X7 Nucleotide Receptor is Coupled to GSK-3 Inhibition and Neuroprotection in Cerebellar Granule Neurons

et al. 2009

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“…More recently, we showed that intranasal administration of rhIGF-1 for 2 weeks, in order to promote IGF-1 delivery to the brain, enhanced IGF-1 cortical levels and improved motor activity and both peripheral and central metabolic abnormalities in YAC128 mice [30], an animal model presenting high levels of IGF-1 in plasma and expression in the striatum [26]. We also showed that rhIGF-1 intranasal administration in YAC128 mice activated [87]. Also, insulin was shown to inhibit Erk1/2 phosphorylation in a PI-3K-dependent manner in Neuro2a cells [88].…”

Section: Discussionmentioning

confidence: 94%

Insulin and IGF-1 improve mitochondrial function in a PI-3K/Akt-dependent manner and reduce mitochondrial generation of reactive oxygen species in Huntington’s disease knock-in striatal cells

Ribeiro

Rosenstock

Oliveira

et al. 2014

Free Radical Biology and Medicine

120

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Insulin and IGF-1 improve mitochondrial function in a PI-3K/Akt-dependent manner and reduce mitochondrial generation of reactive oxygen species in Huntington's disease knock-in striatal cells, Free Radical Biology and Medicine, http://dx.doi.org/10.1016/j. freeradbiomed.2014.06.023 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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“…Therefore, hemoglobin might exist in non-erythroid cells and fulfill alternative function. Akap1 encodes an anchoring protein widely expressed in brain (McKee et al 2005) and crucial for cAMP/PKA signaling (Newhall et al 2006), a pathway which mediates the anti-apoptotic activity of IGF1 on cerebellum granular neurons (Subramaniam et al 2005). The downregulation of cdh1, encoding E-cadherin, should also influence granular cell cycling and differentiation (Almeida et al 2005).…”

Section: Discussionmentioning

confidence: 99%

A combined approach identifies a limited number of new thyroid hormone target genes in post-natal mouse cerebellum

Quignodon¹,

Grijota-Martínez²,

Compe³

et al. 2007

Journal of Molecular Endocrinology

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Thyroid hormones act directly on gene transcription in the post-natal developing cerebellum, controlling neuronal, and glial cell differentiation. We have combined three experimental approaches to identify the target genes that are underlying this phenomenon: 1) a microarray analysis of gene expression to identify hormone responsive genes in the cerebellum of Pax8 K/K mice, a transgenic mouse model of congenital hypothyroidism; 2) a similar microarray analysis on primary culture of cerebellum neurons; and 3) a bioinformatics screen of conserved putative-binding sites in the mouse genome. This identifies surprisingly a small set of target genes, which, for some of them, might be key regulators of cerebellum development and neuronal differentiation.

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Insulin-Like Growth Factor 1 Inhibits Extracellular Signal-Regulated Kinase to Promote Neuronal Survival via the Phosphatidylinositol 3-Kinase/Protein Kinase A/c-Raf Pathway

Cited by 85 publications

References 76 publications

P2X7 Nucleotide Receptor is Coupled to GSK-3 Inhibition and Neuroprotection in Cerebellar Granule Neurons

P2X7 Nucleotide Receptor is Coupled to GSK-3 Inhibition and Neuroprotection in Cerebellar Granule Neurons

Insulin and IGF-1 improve mitochondrial function in a PI-3K/Akt-dependent manner and reduce mitochondrial generation of reactive oxygen species in Huntington’s disease knock-in striatal cells

A combined approach identifies a limited number of new thyroid hormone target genes in post-natal mouse cerebellum

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