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Philip A. Barker - One of the best experts on this subject based on the ideXlab platform.
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p75 Neurotrophin Receptor reduces ligand-induced Trk Receptor ubiquitination and delays Trk Receptor internalization and degradation
EMBO reports, 2005Co-Authors: Joe P S Makkerh, Claire Ceni, Daniel S. Auld, François Vaillancourt, Geneviève Dorval, Philip A. BarkerAbstract:Target-derived Neurotrophins regulate neuronal survival and growth by interacting with cell-surface tyrosine kinase Receptors. The p75 Neurotrophin Receptor (p75NTR) is coexpressed with Trk Receptors in long-range projection neurons, in which it facilitates Neurotrophin binding to Trk and enhances Trk activity. Here, we show that TrkA and TrkB Receptors undergo robust ligand-dependent ubiquitination that is dependent on activation of the endogenous Trk activity of the Receptors. Coexpression of p75NTR attenuated ubiquitination of TrkA and TrkB and delayed nerve growth factor-induced TrkA Receptor internalization and Receptor degradation. These results indicate that p75NTR may prolong cell-surface Trk-dependent signalling events by negatively regulating Receptor ubiquitination.
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the p75 Neurotrophin Receptor multiple interactors and numerous functions
Progress in Brain Research, 2004Co-Authors: Jennifer J Gentry, Philip A. Barker, Bruce D. CarterAbstract:The Neurotrophin Receptor p75 (p75NTR), is involved in a diverse array of cellular responses, including apoptosis, neurite outgrowth and myelination. Stimulation of p75NTR with Neurotrophin can activate multiple downstream signals, including the small GTP binding protein Rac, the transcription factor NF-kappa B and the stress activated kinase, JNK. How these signals are generated and regulated to produce a specific cellular effect has yet to be fully elucidated. A number of proteins have recently been shown to interact with the intracellular domain of p75NTR. Here, we review these p75NTR interacting factors and the current evidence as to how they contribute to the functional effects of p75NTR activation.
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Neurotrophin signaling through the p75 Neurotrophin Receptor
Progress in Neurobiology, 2002Co-Authors: Philippe P Roux, Philip A. BarkerAbstract:The Neurotrophins are growth factors that play critical roles in the development, maintenance, survival, and death of the nervous system. The signal transducing systems that mediate the diverse biological functions of the Neurotrophins are initiated by their interactions with two categories of cell surface Receptors, the Trk family of tyrosine kinases and the p75 Neurotrophin Receptor (p75NTR). While the Trk Receptors are responsible for most of the survival and growth properties of the Neurotrophins, the actions of p75NTR fall into two categories. First, p75NTR is a Trk co-Receptor that can enhance or suppress Neurotrophin-mediated Trk Receptor activity. Second, p75NTR autonomously activates signaling cascades that result in the induction of apoptosis or in the promotion of survival. The signaling cascades activated by p75NTR remain elusive, but structural and functional differences between p75NTR and other tumor necrosis factor Receptor (TNFR) superfamily members suggest that p75NTR employs distinct signaling pathways. p75NTR has been shown to activate the NF-kappaB, Akt, and JNK pathways and interacts with several adaptor proteins. Of these, NRAGE, NADE, and NRIF have been associated with the induction of apoptosis, and FAP-1, RIP2, and TRAF6 appear to promote cellular survival. It remains a major challenge to link the various p75NTR binding proteins to specific p75NTR-dependent functions, but the identification of p75NTR interactors and signaling pathways has sparked new directions in p75NTR research, and will provide a better understanding of this enigmatic Receptor.
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nrage a novel mage protein interacts with the p75 Neurotrophin Receptor and facilitates nerve growth factor dependent apoptosis
Neuron, 2000Co-Authors: Amir H Salehi, Philippe P Roux, Chris J Kubu, Christine Zeindler, Asha L Bhakar, Lauralee Tannis, Joseph M Verdi, Philip A. BarkerAbstract:Abstract The mechanisms employed by the p75 Neurotrophin Receptor (p75NTR) to mediate Neurotrophin-dependent apoptosis are poorly defined. Two-hybrid analyses were used to identify proteins involved in p75NTR apoptotic signaling, and a p75NTR binding partner termed NRAGE (for Neurotrophin Receptor–interacting MAGE homolog) was identified. NRAGE binds p75NTR in vitro and in vivo, and NRAGE associates with the plasma membrane when NGF is bound to p75NTR. NRAGE blocks the physical association of p75NTR with TrkA, and, conversely, TrkA overexpression eliminates NRAGE-mediated NGF-dependent death, indicating that interactions of NRAGE or TrkA with p75NTR are functionally and physically exclusive. NRAGE overexpression facilitates cell cycle arrest and permits NGF-dependent apoptosis within sympathetic neuron precursors cells. Our results show that NRAGE contributes to p75NTR-dependent cell death and suggest novel functions for MAGE family proteins.
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p75 Neurotrophin Receptor expression is induced in apoptotic neurons after seizure
The Journal of Neuroscience, 1999Co-Authors: Philippe P Roux, Philip A. Barker, Michael A Colicos, Timothy E KennedyAbstract:Seizure causes neuronal cell loss in both animal models and human epilepsy. To determine the contribution of apoptotic mechanisms to seizure-induced neuronal cell death, rat brains were examined for the occurrence of terminal deoxynucleotidyl transferase-mediated UTP nick end labeling (TUNEL)-positive nuclei after pilocarpine-induced seizure. Numerous TUNEL-positive cells were observed throughout the postseizure hippocampus, piriform cortex, and entorhinal cortex. Combined TUNEL/NeuN immunocytochemistry demonstrated that the vast majority of TUNEL-positive cells were neurons. To identify components of the signal transduction cascade promoting postseizure apoptosis, the expression of the p75 Neurotrophin Receptor (p75NTR) was examined. Seizure-induced increases in p75NTR protein and mRNA were detected in hippocampus, piriform cortex, and entorhinal cortex. Immunohistochemical double labeling revealed almost complete correspondence between TUNEL-positive and p75NTR-expressing cells, suggesting that seizure-induced neuronal loss within the CNS occurs through apoptotic signaling cascades involving p75NTR.
Yves-alain Barde - One of the best experts on this subject based on the ideXlab platform.
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the p75 Neurotrophin Receptor negatively modulates dendrite complexity and spine density in hippocampal neurons
The Journal of Neuroscience, 2005Co-Authors: Martha Zagrebelsky, Georg Dechant, Yves-alain Barde, Andreas Holz, Tobias Bonhoeffer, Martin KorteAbstract:The correlation between functional and structural neuronal plasticity is by now well documented. However, the molecular mechanisms translating patterns of neuronal activity into specific changes in the structure of neurons remain unclear. Neurotrophins can be released in an activity-dependent manner, and they are capable of controlling both neuronal morphology and functional synaptic changes. They are thus attractive molecules to be studied in the context of synaptic plasticity. In the CNS, most of the work so far has focused on the role of BDNF and of its tyrosine kinase B Receptor (TrkB), but relatively little is known about the function of the pan-Neurotrophin Receptor p75NTR. In this study, we show in loss-of-function experiments that postnatal hippocampal pyramidal cells in two mutant lines of p75NTR have a higher spine density and greater dendritic complexity than wild-type (WT) mice. Conversely, in a gain-of-function approach, p75NTR overexpression in WT neurons significantly reduces dendritic complexity, as well as spine density in all dendritic compartments. These results show that p75NTR negatively modulates dendritic morphology in adult hippocampal pyramidal neurons and documents a new case of functional antagonism between Trk and p75NTR signaling.
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The Neurotrophin Receptor p75^NTR: novel functions and implications for diseases of the nervous system
Nature Neuroscience, 2002Co-Authors: Georg Dechant, Yves-alain BardeAbstract:Neurotrophins have long been known to promote the survival and differentiation of vertebrate neurons. However, these growth factors can also induce cell death through the p75 Neurotrophin Receptor (p75^NTR), a member of the tumor necrosis factor Receptor superfamily. Consistent with a function in controlling the survival and process formation of neurons, p75^NTR is mainly expressed during early neuronal development. In the adult, p75^NTR is re-expressed in various pathological conditions, including epilepsy, axotomy and neurodegeneration. Potentially toxic peptides, including the amyloid β- (Aβ-) peptide that accumulates in Alzheimer's disease, are ligands for p75^NTR. Recent work also implicates p75^NTR in the regulation of both synaptic transmission and axonal elongation. It associates with the Nogo Receptor, a binding protein for axonal growth inhibitors, and appears to be the transducing subunit of this Receptor complex.
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the Neurotrophin Receptor p75 ntr novel functions and implications for diseases of the nervous system
Nature Neuroscience, 2002Co-Authors: Georg Dechant, Yves-alain BardeAbstract:Neurotrophins have long been known to promote the survival and differentiation of vertebrate neurons. However, these growth factors can also induce cell death through the p75 Neurotrophin Receptor (p75(NTR)), a member of the tumor necrosis factor Receptor superfamily. Consistent with a function in controlling the survival and process formation of neurons, p75(NTR) is mainly expressed during early neuronal development. In the adult, p75(NTR) is re-expressed in various pathological conditions, including epilepsy, axotomy and neurodegeneration. Potentially toxic peptides, including the amyloid beta- (Abeta-) peptide that accumulates in Alzheimer's disease, are ligands for p75(NTR). Recent work also implicates p75(NTR) in the regulation of both synaptic transmission and axonal elongation. It associates with the Nogo Receptor, a binding protein for axonal growth inhibitors, and appears to be the transducing subunit of this Receptor complex.
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the zinc finger protein nrif interacts with the Neurotrophin Receptor p75ntr and participates in programmed cell death
The EMBO Journal, 1999Co-Authors: Elisabeth Casademunt, José María Frade, Bruce D. Carter, Georg Dechant, Isabel Benzel, Yves-alain BardeAbstract:NRIF (Neurotrophin Receptor interacting factor) is a ubiquitously expressed zinc finger protein of the Kruppel family which interacts with the Neurotrophin Receptor p75(NTR). The interaction was first detected in yeast and then biochemically confirmed using recombinant GST-NRIF fusions and p75(NTR) expressed by eukaryotic cells. Transgenic mice carrying a deletion in the exon encoding the p75(NTR)-binding domain of NRIF display a phenotype which is strongly dependent upon genetic background. While at the F(2 )generation there is only limited (20%) embryonic lethality, in a congenic BL6 strain nrif(-/-) mice cannot survive beyond E12, but are viable and healthy to adulthood in the Sv129 background. The involvement of NRIF in p75(NTR)/NGF-mediated developmental cell death was examined in the mouse embryonic neural retina. Disruption of the nrif gene leads to a reduction in cell death which is quantitatively indistinguishable from that observed in p75(NTR)(-/-) and ngf(-/-) mice. These results indicate that NRIF is an intracellular p75(NTR)-binding protein transducing cell death signals during development.
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Signalling through the Neurotrophin Receptor p75NTR.
Current opinion in neurobiology, 1997Co-Authors: Georg Dechant, Yves-alain BardeAbstract:Activation specific tyrosine kinase Receptors by Neurotrophins accounts for the longest known biological actions of the Neurotrophins, in particular the promotion of neuronal survival. However, recent studies have revealed that nerve growth factor, the Neurotrophin regarded as best understood, also activates a signalling pathway by binding to the Neurotrophin Receptor p75(NTR). This Receptor belongs to the tumor necrosis factor Receptor family and lacks intrinsic catalytic activity. The p75(NTR) Receptor binds all Neurotrophins with nanomolar affinity; however, nerve growth factor seems to be uniquely able to activate it, causing the death of trkA-negative neurons during normal development. Thus, nerve growth factor prevents programmed cell death through its Receptor TrkA, but promotes it by signalling through p75(NTR).
Bruce D. Carter - One of the best experts on this subject based on the ideXlab platform.
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the biological functions and signaling mechanisms of the p75 Neurotrophin Receptor
Handbook of experimental pharmacology, 2014Co-Authors: Sung Ok Yoon, Bruce D. Carter, B R KraemerAbstract:The p75 Neurotrophin Receptor (p75NTR) regulates a wide range of cellular functions, including programmed cell death, axonal growth and degeneration, cell proliferation, myelination, and synaptic plasticity. The multiplicity of cellular functions governed by the Receptor arises from the variety of ligands and co-Receptors which associate with p75NTR and regulate its signaling. P75NTR promotes survival through interactions with Trk Receptors, inhibits axonal regeneration via partnerships with Nogo Receptor (Nogo-R) and Lingo-1, and promotes apoptosis through association with Sortilin. Signals downstream of these interactions are further modulated through regulated intramembrane proteolysis (RIP) of p75NTR and by interactions with numerous cytosolic partners. In this chapter, we discuss the intricate signaling mechanisms of p75NTR, emphasizing how these signals are differentially regulated to mediate these diverse cellular functions.
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induction of proNeurotrophins and activation of p75ntr mediated apoptosis via Neurotrophin Receptor interacting factor in hippocampal neurons after seizures
The Journal of Neuroscience, 2008Co-Authors: Marta Volosin, Barbara L. Hempstead, Bruce D. Carter, Christy Trotter, Andrea B Cragnolini, Rajappa S Kenchappa, Matthew Light, Wilma J FriedmanAbstract:Seizure-induced damage elicits a loss of hippocampal neurons mediated to a great extent by the p75 Neurotrophin Receptor (NTR). ProNeurotrophins, which are potent apoptosis-inducing ligands for p75NTR, were increased in the hippocampus, particularly in astrocytes, by pilocarpine-induced seizures; and infusion of anti-pro-NGF dramatically attenuated neuronal loss after seizures. The p75NTR is expressed in many different cell types in the nervous system, and can mediate a variety of different cellular functions by recruiting specific intracellular binding proteins to activate distinct signaling pathways. In this study, we demonstrate that Neurotrophin Receptor-interacting factor (NRIF) mediates apoptotic signaling via p75NTR in hippocampal neurons in vitro and in vivo . After seizure-induced injury, NRIF −/− mice showed an increase in p75NTR expression in the hippocampus; however, these neurons failed to undergo apoptosis in contrast to wild-type mice. Treatment of cultured hippocampal neurons with proNeurotrophins induced association of NRIF with p75NTR and subsequent translocation of NRIF to the nucleus, which was dependent on cleavage of the Receptor. Neurons lacking NRIF were resistant to p75NTR-mediated apoptosis in vitro and in vivo . In addition, we demonstrate some mechanistic differences in p75NTR signaling in hippocampal neurons compared with other cell types. Overall, these studies demonstrate the requirement for NRIF to signal p75NTR-mediated apoptosis of hippocampal neurons and that blocking pro-NGF can inhibit neuronal loss after seizures.
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Neurotrophin Receptor Interacting Factor (NRIF) Is an Essential Mediator of Apoptotic Signaling by the p75 Neurotrophin Receptor
The Journal of biological chemistry, 2005Co-Authors: Michelle S. Linggi, Tara L. Burke, B. Blairanne Williams, Anthony W. Harrington, Rosemary Kraemer, Barbara L. Hempstead, Sung Ok Yoon, Bruce D. CarterAbstract:Activation of the p75 Neurotrophin Receptor leads to a variety of effects within the nervous system, including neuronal apoptosis. Both c-Jun N-terminal kinase (JNK) and the tumor suppressor p53 have been reported to be critical for this Receptor to induce cell death; however, the mechanisms by which p75 activates these pathways is undetermined. Here we report that the Neurotrophin Receptor interacting factor (NRIF) is necessary for p75-dependent JNK activation and apoptosis. Upon nerve growth factor withdrawal, nrif-/- sympathetic neurons underwent apoptosis, whereas p75-mediated death was completely abrogated. The lack of cell death correlated with a lack of JNK activation in the nrif-/- neurons, suggesting that NRIF is a selective mediator for p75-dependent JNK activation and apoptosis. Moreover, we document that NRIF expression is sufficient to induce cell death through a mechanism that requires p53. Taken together, these results establish NRIF as an essential component of the p75 apoptotic pathway.
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the p75 Neurotrophin Receptor multiple interactors and numerous functions
Progress in Brain Research, 2004Co-Authors: Jennifer J Gentry, Philip A. Barker, Bruce D. CarterAbstract:The Neurotrophin Receptor p75 (p75NTR), is involved in a diverse array of cellular responses, including apoptosis, neurite outgrowth and myelination. Stimulation of p75NTR with Neurotrophin can activate multiple downstream signals, including the small GTP binding protein Rac, the transcription factor NF-kappa B and the stress activated kinase, JNK. How these signals are generated and regulated to produce a specific cellular effect has yet to be fully elucidated. A number of proteins have recently been shown to interact with the intracellular domain of p75NTR. Here, we review these p75NTR interacting factors and the current evidence as to how they contribute to the functional effects of p75NTR activation.
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the zinc finger protein nrif interacts with the Neurotrophin Receptor p75ntr and participates in programmed cell death
The EMBO Journal, 1999Co-Authors: Elisabeth Casademunt, José María Frade, Bruce D. Carter, Georg Dechant, Isabel Benzel, Yves-alain BardeAbstract:NRIF (Neurotrophin Receptor interacting factor) is a ubiquitously expressed zinc finger protein of the Kruppel family which interacts with the Neurotrophin Receptor p75(NTR). The interaction was first detected in yeast and then biochemically confirmed using recombinant GST-NRIF fusions and p75(NTR) expressed by eukaryotic cells. Transgenic mice carrying a deletion in the exon encoding the p75(NTR)-binding domain of NRIF display a phenotype which is strongly dependent upon genetic background. While at the F(2 )generation there is only limited (20%) embryonic lethality, in a congenic BL6 strain nrif(-/-) mice cannot survive beyond E12, but are viable and healthy to adulthood in the Sv129 background. The involvement of NRIF in p75(NTR)/NGF-mediated developmental cell death was examined in the mouse embryonic neural retina. Disruption of the nrif gene leads to a reduction in cell death which is quantitatively indistinguishable from that observed in p75(NTR)(-/-) and ngf(-/-) mice. These results indicate that NRIF is an intracellular p75(NTR)-binding protein transducing cell death signals during development.
Georg Dechant - One of the best experts on this subject based on the ideXlab platform.
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the p75 Neurotrophin Receptor negatively modulates dendrite complexity and spine density in hippocampal neurons
The Journal of Neuroscience, 2005Co-Authors: Martha Zagrebelsky, Georg Dechant, Yves-alain Barde, Andreas Holz, Tobias Bonhoeffer, Martin KorteAbstract:The correlation between functional and structural neuronal plasticity is by now well documented. However, the molecular mechanisms translating patterns of neuronal activity into specific changes in the structure of neurons remain unclear. Neurotrophins can be released in an activity-dependent manner, and they are capable of controlling both neuronal morphology and functional synaptic changes. They are thus attractive molecules to be studied in the context of synaptic plasticity. In the CNS, most of the work so far has focused on the role of BDNF and of its tyrosine kinase B Receptor (TrkB), but relatively little is known about the function of the pan-Neurotrophin Receptor p75NTR. In this study, we show in loss-of-function experiments that postnatal hippocampal pyramidal cells in two mutant lines of p75NTR have a higher spine density and greater dendritic complexity than wild-type (WT) mice. Conversely, in a gain-of-function approach, p75NTR overexpression in WT neurons significantly reduces dendritic complexity, as well as spine density in all dendritic compartments. These results show that p75NTR negatively modulates dendritic morphology in adult hippocampal pyramidal neurons and documents a new case of functional antagonism between Trk and p75NTR signaling.
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The Neurotrophin Receptor p75^NTR: novel functions and implications for diseases of the nervous system
Nature Neuroscience, 2002Co-Authors: Georg Dechant, Yves-alain BardeAbstract:Neurotrophins have long been known to promote the survival and differentiation of vertebrate neurons. However, these growth factors can also induce cell death through the p75 Neurotrophin Receptor (p75^NTR), a member of the tumor necrosis factor Receptor superfamily. Consistent with a function in controlling the survival and process formation of neurons, p75^NTR is mainly expressed during early neuronal development. In the adult, p75^NTR is re-expressed in various pathological conditions, including epilepsy, axotomy and neurodegeneration. Potentially toxic peptides, including the amyloid β- (Aβ-) peptide that accumulates in Alzheimer's disease, are ligands for p75^NTR. Recent work also implicates p75^NTR in the regulation of both synaptic transmission and axonal elongation. It associates with the Nogo Receptor, a binding protein for axonal growth inhibitors, and appears to be the transducing subunit of this Receptor complex.
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the Neurotrophin Receptor p75 ntr novel functions and implications for diseases of the nervous system
Nature Neuroscience, 2002Co-Authors: Georg Dechant, Yves-alain BardeAbstract:Neurotrophins have long been known to promote the survival and differentiation of vertebrate neurons. However, these growth factors can also induce cell death through the p75 Neurotrophin Receptor (p75(NTR)), a member of the tumor necrosis factor Receptor superfamily. Consistent with a function in controlling the survival and process formation of neurons, p75(NTR) is mainly expressed during early neuronal development. In the adult, p75(NTR) is re-expressed in various pathological conditions, including epilepsy, axotomy and neurodegeneration. Potentially toxic peptides, including the amyloid beta- (Abeta-) peptide that accumulates in Alzheimer's disease, are ligands for p75(NTR). Recent work also implicates p75(NTR) in the regulation of both synaptic transmission and axonal elongation. It associates with the Nogo Receptor, a binding protein for axonal growth inhibitors, and appears to be the transducing subunit of this Receptor complex.
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complete ablation of the Neurotrophin Receptor p75ntr causes defects both in the nervous and the vascular system
Nature Neuroscience, 2001Co-Authors: David Von Schack, Elisabeth Casademunt, Rudiger Schweigreiter, Michael Meyer, Miriam Bibel, Georg DechantAbstract:We identified a protein isoform of the common Neurotrophin Receptor p75NTR that arises from alternative splicing of exon III in the p75NTR locus. Because this protein is left intact in the previously described p75NTR mutant mouse line1, we generated a new p75NTR mutant allele. Mice homozygous for this mutation lack both protein isoforms, display severe nervous system defects and reveal a previously unknown role of p75NTR in the formation of blood vessels.
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the zinc finger protein nrif interacts with the Neurotrophin Receptor p75ntr and participates in programmed cell death
The EMBO Journal, 1999Co-Authors: Elisabeth Casademunt, José María Frade, Bruce D. Carter, Georg Dechant, Isabel Benzel, Yves-alain BardeAbstract:NRIF (Neurotrophin Receptor interacting factor) is a ubiquitously expressed zinc finger protein of the Kruppel family which interacts with the Neurotrophin Receptor p75(NTR). The interaction was first detected in yeast and then biochemically confirmed using recombinant GST-NRIF fusions and p75(NTR) expressed by eukaryotic cells. Transgenic mice carrying a deletion in the exon encoding the p75(NTR)-binding domain of NRIF display a phenotype which is strongly dependent upon genetic background. While at the F(2 )generation there is only limited (20%) embryonic lethality, in a congenic BL6 strain nrif(-/-) mice cannot survive beyond E12, but are viable and healthy to adulthood in the Sv129 background. The involvement of NRIF in p75(NTR)/NGF-mediated developmental cell death was examined in the mouse embryonic neural retina. Disruption of the nrif gene leads to a reduction in cell death which is quantitatively indistinguishable from that observed in p75(NTR)(-/-) and ngf(-/-) mice. These results indicate that NRIF is an intracellular p75(NTR)-binding protein transducing cell death signals during development.
Eero Castrén - One of the best experts on this subject based on the ideXlab platform.
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mapping of the interaction site between sortilin and the p75 Neurotrophin Receptor reveals a regulatory role for the sortilin intracellular domain in p75 Neurotrophin Receptor shedding and apoptosis
Journal of Biological Chemistry, 2012Co-Authors: Alex M Sykes, Sune Skeldal, Simon Glerup, Dusan Matusica, Nickless Palstra, Henri Autio, Zoran Boskovic, Peder Madsen, Eero CastrénAbstract:Neurotrophins comprise a group of neuronal growth factors that are essential for the development and maintenance of the nervous system. However, the immature pro-Neurotrophins promote apoptosis by engaging in a complex with sortilin and the p75 Neurotrophin Receptor (p75NTR). To identify the interaction site between sortilin and p75NTR, we analyzed binding between chimeric Receptor constructs and truncated p75NTR variants by co-immunoprecipitation experiments, surface plasmon resonance analysis, and FRET. We found that complex formation between sortilin and p75NTR relies on contact points in the extracellular domains of the Receptors. We also determined that the interaction critically depends on an extracellular juxtamembrane 23-amino acid sequence of p75NTR. Functional studies further revealed an important regulatory function of the sortilin intracellular domain in p75NTR-regulated intramembrane proteolysis and apoptosis. Thus, although the intracellular domain of sortilin does not contribute to p75NTR binding, it does regulate the rates of p75NTR cleavage, which is required to mediate pro-Neurotrophin-stimulated cell death.
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Phosphoproteomic Analysis of Neurotrophin Receptor TrkB Signaling Pathways in Mouse Brain
Cellular and molecular neurobiology, 2006Co-Authors: Artour Semenov, Gundars Goldsteins, Eero CastrénAbstract:1. The signaling pathways activated by trkB Neurotrophin Receptor have been studied in detail in cultured neurons, but little is known about the pathways activated by trkB in intact brain. TrkB is a tyrosine kinase and protein phosphorylation is a key regulatory process in the neuronal signal transduction pathways.