Proteomic Approaches to Dissect Neuronal Signaling Pathways

2014 ◽  
pp. 499-508 ◽  
Author(s):  
Heather L. Bowling ◽  
Katrin Deinhardt
Keyword(s):  
Signaling Pathways ◽  
Neuronal Signaling

scholarly journals Differential Signaling Mediated by ApoE2, ApoE3, and ApoE4 in Human Neurons Parallels Alzheimer’s Disease Risk

2018 ◽  
Author(s):  
Yu-Wen Alvin Huang ◽  
Bo Zhou ◽  
Amber M. Nabet ◽  
Marius Wernig ◽  
Thomas C. Südhof
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Signaling Pathways ◽  
Synapse Formation ◽  
Disease Risk ◽  
Rank Order ◽  
Neuronal Signaling ◽  
Differential Signaling ◽  
Human Neurons ◽  
Apoe Receptor

AbstractApolipoprotein E (ApoE) mediates clearance of circulating lipoproteins from blood by binding to ApoE receptors. Humans express three genetic variants, ApoE2, ApoE3, and ApoE4, that exhibit distinct ApoE receptor binding properties. In brain, ApoE is abundantly produced by activated astrocytes and microglia, and three variants differentially affect Alzheimer’s disease (AD), such that ApoE2 protects against, and ApoE4 predisposes to the disease. A role for ApoE4 in driving microglial dysregulation and impeding Aβ clearance in AD is well documented, but the direct effects of three variants on neurons are poorly understood. Extending previous studies, we here demonstrate that ApoE variants differentially activate multiple neuronal signaling pathways and regulate synaptogenesis. Specifically, using human neurons cultured in the absence of glia to exclude indirect glial mechanisms, we show that ApoE broadly stimulates signal transduction cascades which among others enhance synapse formation with an ApoE4>ApoE3>ApoE2 potency rank order, paralleling the relative risk for AD conferred by these variants. Unlike the previously described induction of APP transcription, however, ApoE-induced synaptogenesis involves CREB rather than cFos activation. We thus propose that in brain, ApoE acts as a glia-secreted paracrine signal and activates neuronal signaling pathways in what may represent a protective response, with the differential potency of ApoE variants causing distinct levels of chronic signaling that may contribute to AD pathogenesis.

Genomic regions underlying metabolic and neuronal signaling pathways are temporally consistent in a moving avian hybrid zone

Evolution ◽  
2020 ◽  
Vol 74 (7) ◽  
pp. 1498-1513
Author(s):  
Dominique N. Wagner ◽  
Robert L. Curry ◽  
Nancy Chen ◽  
Irby J. Lovette ◽  
Scott A. Taylor
Keyword(s):  
Signaling Pathways ◽  
Hybrid Zone ◽  
Neuronal Signaling ◽  
Genomic Regions

Presynaptic Ca2+ channels – integration centers for neuronal signaling pathways

2006 ◽  
Vol 29 (11) ◽  
pp. 617-624 ◽  
Author(s):  
Rhian M. Evans ◽  
Gerald W. Zamponi
Keyword(s):  
Signaling Pathways ◽  
Neuronal Signaling ◽  
Ca2 Channels

scholarly journals Genome-Wide Identification of Calcium-Response Factor (CaRF) Binding Sites Predicts a Role in Regulation of Neuronal Signaling Pathways

PLoS ONE ◽  
2010 ◽  
Vol 5 (5) ◽  
pp. e10870 ◽  
Author(s):  
Andreas R. Pfenning ◽  
Tae-Kyung Kim ◽  
James M. Spotts ◽  
Martin Hemberg ◽  
Dan Su ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Binding Sites ◽  
Response Factor ◽  
Calcium Response ◽  
Neuronal Signaling ◽  
Genome Wide

scholarly journals Neuronal signaling pathways: genetic insights into the pathophysiology of major mental illness

2009 ◽  
Vol 35 (1) ◽  
pp. 350-351 ◽  
Author(s):  
Russell L Margolis ◽  
Christopher A Ross
Keyword(s):  
Mental Illness ◽  
Signaling Pathways ◽  
Neuronal Signaling

Antagonistic roles for STYX pseudophosphatases in neurite outgrowth

2017 ◽  
Vol 45 (2) ◽  
pp. 381-387 ◽  
Author(s):  
Arya Dahal ◽  
Shantá D. Hinton
Keyword(s):  
Signaling Pathways ◽  
Neurite Outgrowth ◽  
Neuronal Development ◽  
Mitogen Activated Protein Kinases ◽  
Neuronal Signaling ◽  
Stress Response Pathway ◽  
Mitogen Activated Protein ◽  
Neuronal Processes ◽  
Mapk Phosphatases ◽  
Lateral Sclerosis

Mitogen-activated protein kinases (MAPKs) are essential players in important neuronal signaling pathways including neuronal development, plasticity, survival, learning, and memory. The inactivation of MAPKs is tightly controlled by MAPK phosphatases (MKPs), which also are important regulators of these neuronal processes. Considering that MAPKs and MKPs are major players in neuronal signaling, it follows that their misregulation is pivotal in neurodegenerative diseases such as Alzheimer's, Huntington's, Parkinson's, and amyotrophic lateral sclerosis. In contrast, the actions of their noncatalytic homologs, or pseudoenzymes, have received minimal attention as important regulators in neuronal signaling pathways and relevant diseases. There is compelling evidence, however, that pseudophosphatases, such as STYX (phospho-serine–threonine/tyrosine-binding protein) and MAPK-STYX (MK-STYX), are integral signaling molecules in regulating pathways involved in neuronal developmental processes such as neurite outgrowth. Here, we discuss how the dynamics of MK-STYX in the stress response pathway imply that this unique member of the MKP subfamily has the potential to have a major role in neuronal signaling. We further compare the actions of STYX in preventing neurite-like outgrowths and MK-STYX in inducing neurite outgrowths. The roles of these pseudophosphatases in neurite outgrowth highlight their emergence as important candidates to investigate in neurodegenerative disorders and diseases.

scholarly journals Pleiotropic Role Played by the PDZ Domain in Neuronal Signaling Pathways

2016 ◽  
Vol 110 (3) ◽  
pp. 362a
Author(s):  
Célia Caillet-Saguy ◽  
Pierre Maisonneuve ◽  
Florent Delhommel ◽  
Henri Buc ◽  
Monique Lafon ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Pdz Domain ◽  
Neuronal Signaling
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