ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999
Akt-dependent potentiation of L channels by insulin-like growth factor-1 is required for neuronal survival.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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The trial behind it
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Who cites it
38 citing papers in PubMed, 137 citations in OpenAlex.
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- Original Research: Polyphenols extracted from grape powder induce lipogenesis and glucose uptake during differentiation of murine preadipocytes.Experimental biology and medicine (Maywood, N.J.) · 2016Article
- Control of cardiac repolarization by phosphoinositide 3-kinase signaling to ion channels.Circulation research · 2015Review
- Nerve growth factor (NGF) regulates activity of nuclear factor of activated T-cells (NFAT) in neurons via the phosphatidylinositol 3-kinase (PI3K)-Akt-glycogen synthase kinase 3β (GSK3β) pathway.The Journal of biological chemistry · 2014Article
- The CNS glucagon-like peptide-2 receptor in the control of energy balance and glucose homeostasis.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Review
- Article
- Insulin-like growth factor-1 in CNS and cerebrovascular aging.Frontiers in aging neuroscience · 2013Article
- Aging, synaptic dysfunction, and insulin-like growth factor (IGF)-1.The journals of gerontology. Series A, Biological sciences and medical sciences · 2012Review
- PI3-kinase/Akt pathway-regulated membrane insertion of acid-sensing ion channel 1a underlies BDNF-induced pain hypersensitivity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- α7 nicotinic ACh receptors as a ligand-gated source of Ca(2+) ions: the search for a Ca(2+) optimum.Advances in experimental medicine and biology · 2012Review
- Phosphorylation of neuronal survival factor MEF2D by glycogen synthase kinase 3beta in neuronal apoptosis.The Journal of biological chemistry · 2009Article
- IGF-1 and pAKT signaling promote hippocampal CA1 neuronal survival following injury to dentate granule cells.Neurotoxicity research · 2009Article
- Growth factor-dependent trafficking of cerebellar NMDA receptors via protein kinase B/Akt phosphorylation of NR2C.Neuron · 2009Article
- Akt regulates L-type Ca2+ channel activity by modulating Cavalpha1 protein stability.The Journal of cell biology · 2009Article
- Phosphatidylinositol 3 kinase-Akt signaling serves as a circadian output in the retina.Journal of neurochemistry · 2009Article
- Sensory perception of food and insulin-like signals influence seizure susceptibility.PLoS genetics · 2008Article
- Estrogen receptor protein interaction with phosphatidylinositol 3-kinase leads to activation of phosphorylated Akt and extracellular signal-regulated kinase 1/2 in the same population of cortical neurons: a unified mechanism of estrogen action.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Insulin-like growth factor-1 modulation of CaV1.3 calcium channels depends on Ca2+ release from IP3-sensitive stores and calcium/calmodulin kinase II phosphorylation of the alpha1 subunit EF hand.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Complex regulation of spiral ganglion neuron firing patterns by neurotrophin-3.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The insulin-like growth factor-1 (IGF-1)/receptor tyrosine kinase recently has been shown to mediate neuronal survival and potentiate the activity of specific calcium channel subtypes; survival requires Akt, a serine/threonine kinase. We demonstrate here that Akt mediates the IGF-1-induced potentiation of L channel currents, but not that of N channels. Transient expression of wild-type, dominant-negative, and constitutively active forms of Akt in cerebellar granule neurons causes, respectively, no change in IGF-1/L channel potentiation, complete inhibition of potentiation, and a dramatic increase in basal L currents accompanied by the loss of ability to induce further increases. In no case is the IGF-1 potentiation of N currents affected. We additionally find that IGF-1 partially mediates granule neuron survival via L channel activity and that Akt-dependent L channel modulation is a necessary component. Interestingly, very brief exposure (1 min) to IGF-1 triggers nearly complete survival and requires L channel activity. These results strongly suggest that neuronal receptor tyrosine kinases can control long-term calcium-dependent processes via the rapid control of voltage-sensitive channels.
Indexed as
Identifiers
10066247PMC6782565W1586088169What OpenQuestion holds
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.