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Frontiers in Molecular Neuroscience

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https://www.readbyqxmd.com/read/28713243/synaptic-interactome-mining-reveals-p140cap-as-a-new-hub-for-psd-proteins-involved-in-psychiatric-and-neurological-disorders
#1
Annalisa Alfieri, Oksana Sorokina, Annie Adrait, Costanza Angelini, Isabella Russo, Alessandro Morellato, Michela Matteoli, Elisabetta Menna, Elisabetta Boeri Erba, Colin McLean, J Douglas Armstrong, Ugo Ala, Joseph D Buxbaum, Alfredo Brusco, Yohann Couté, Silvia De Rubeis, Emilia Turco, Paola Defilippi
Altered synaptic function has been associated with neurological and psychiatric conditions including intellectual disability, schizophrenia and autism spectrum disorder (ASD). Amongst the recently discovered synaptic proteins is p140Cap, an adaptor that localizes at dendritic spines and regulates their maturation and physiology. We recently showed that p140Cap knockout mice have cognitive deficits, impaired long-term potentiation (LTP) and long-term depression (LTD), and immature, filopodia-like dendritic spines...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28713242/the-distance-between-n-and-c-termini-of-tau-and-of-ftdp-17-mutants-is-modulated-by-microtubule-interactions-in-living-cells
#2
Cristina Di Primio, Valentina Quercioli, Giacomo Siano, Matteo Rovere, Branislav Kovacech, Michal Novak, Antonino Cattaneo
The microtubule (MT)-associated protein Tau is a natively unfolded protein, involved in a number of neurodegenerative disorders, collectively called tauopathies, aggregating in neurofibrillary tangles (NFT). It is an open question how the conversion from a MT bound molecule to an aggregation-prone Tau species occurs and, also, if and how tauopathy-related mutations affect its behavior in the cell. To address these points, we exploited a genetically encoded FRET sensor based on the full length Tau protein, to monitor in real time Tau conformational changes in different conditions in live cells...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28713241/cold-temperature-encoding-by-cutaneous-trpa1-and-trpm8-carrying-fibers-in-the-mouse
#3
Zoltan Winter, Philipp Gruschwitz, Stephanie Eger, Filip Touska, Katharina Zimmermann
Previous research identified TRPM8 and TRPA1 cold transducers with separate functions, one being functional in the non-noxious range and the second one being a nociceptive transducer. TRPM8-deficient mice present overt deficits in the detection of environmental cool, but not a lack of cold avoidance and TRPA1-deficient mice show clear deficits in some cold nocifensive assays. The extent of TRPA1's contribution to cold sensing in vivo is still unclear, because mice lacking both TRPM8 and TRPA1 (DKO) were described with unchanged cold avoidance from TRPM8(-/-) based on a two-temperature-choice assay and by c-fos measurement...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28713240/the-coordinated-action-of-calcineurin-and-cathepsin-d-protects-against-%C3%AE-synuclein-toxicity
#4
Andreas Aufschnaiter, Lukas Habernig, Verena Kohler, Jutta Diessl, Didac Carmona-Gutierrez, Tobias Eisenberg, Walter Keller, Sabrina Büttner
The degeneration of dopaminergic neurons during Parkinson's disease (PD) is intimately linked to malfunction of α-synuclein (αSyn), the main component of the proteinaceous intracellular inclusions characteristic for this pathology. The cytotoxicity of αSyn has been attributed to disturbances in several biological processes conserved from yeast to humans, including Ca(2+) homeostasis, general lysosomal function and autophagy. However, the precise sequence of events that eventually results in cell death remains unclear...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28713239/increased-white-matter-inflammation-in-aging-and-alzheimer-s-disease-brain
#5
Divya Raj, Zhuoran Yin, Marjolein Breur, Janine Doorduin, Inge R Holtman, Marta Olah, Ietje J Mantingh-Otter, Debby Van Dam, Peter P De Deyn, Wilfred den Dunnen, Bart J L Eggen, Sandra Amor, Erik Boddeke
Chronic neuroinflammation, which is primarily mediated by microglia, plays an essential role in aging and neurodegeneration. It is still unclear whether this microglia-induced neuroinflammation occurs globally or is confined to distinct brain regions. In this study, we investigated microglia activity in various brain regions upon healthy aging and Alzheimer's disease (AD)-related pathology in both human and mouse samples. In purified microglia isolated from aging mouse brains, we found a profound gene expression pattern related to pro-inflammatory processes, phagocytosis, and lipid homeostasis...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28701921/endothelial-monocyte-activating-polypeptide-ii-suppresses-the-in-vitro-glioblastoma-induced-angiogenesis-by-inducing-autophagy
#6
Zhiqing Li, Jun Ma, Libo Liu, Xiaobai Liu, Ping Wang, Yunhui Liu, Zhen Li, Jian Zheng, Jiajia Chen, Wei Tao, Yixue Xue
The obstacle in delivering therapeutics to glioblastoma (GBM) is tumor-induced angiogenesis which leads to the formation of abnormal vessels and a dysfunctional blood-tumor barrier. Here, we elucidated the effect of endothelial-monocyte activating polypeptide II (EMAP II) on the GBM-induced angiogenesis as well as its potential mechanisms. Our results proved that EMAP II inhibited the viability, mitochondrial membrane potential, migration and tube formation of GBM-induced endothelial cells (GECs) by inducing cell autophagy, demonstrated by cell viability assay, JC-1 staining assay, transwell assay and tube formation assay, respectively...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28701920/tlx3-function-in-the-dorsal-root-ganglion-is-pivotal-to-itch-and-pain-sensations
#7
Chengcheng Huang, Fumin Lu, Ping Li, Cheng Cao, Zijing Liu
Itch, a sensation eliciting a desire to scratch, is distinct from but not completely independent of pain. Inspiring achievements have been made in the characterization of itch-related receptors and neurotransmitters, but the molecular mechanisms controlling the development of pruriceptors remain poorly understood. Here, our RNAseq and in situ hybridization data show that the transcription factor Tlx3 is required for the expression of a majority of itch-related molecules in the dorsal root ganglion (DRG). As a result, Tlx3(F/F);Nav1...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28701919/amyloid-%C3%AE-impairs-vesicular-secretion-in-neuronal-and-astrocyte-peptidergic-transmission
#8
Virginia Plá, Neus Barranco, Esther Pozas, Fernando Aguado
Regulated secretion of neuropeptides and neurotrophic factors critically modulates function and plasticity of synapses and circuitries. It is believed that rising amyloid-β (Aβ) concentrations, synaptic dysfunction and network disorganization underlie early phases of Alzheimer's disease (AD). Here, we analyze the impact of soluble Aβ1-42 assemblies on peptidergic secretion in cortical neurons and astrocytes. We show that neurons and astrocytes differentially produce and release carboxypeptidase E (CPE) and secretogranin III (SgIII), two dense-core vesicle (DCV) markers belonging to the regulated secretory pathway...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28701918/striatal-transcriptome-and-interactome-analysis-of-shank3-overexpressing-mice-reveals-the-connectivity-between-shank3-and-mtorc1-signaling
#9
Yeunkum Lee, Sun Gyun Kim, Bokyoung Lee, Yinhua Zhang, Yoonhee Kim, Shinhyun Kim, Eunjoon Kim, Hyojin Kang, Kihoon Han
Mania causes symptoms of hyperactivity, impulsivity, elevated mood, reduced anxiety and decreased need for sleep, which suggests that the dysfunction of the striatum, a critical component of the brain motor and reward system, can be causally associated with mania. However, detailed molecular pathophysiology underlying the striatal dysfunction in mania remains largely unknown. In this study, we aimed to identify the molecular pathways showing alterations in the striatum of SH3 and multiple ankyrin repeat domains 3 (Shank3)-overexpressing transgenic (TG) mice that display manic-like behaviors...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28701917/distinct-features-of-doublecortin-as-a-marker-of-neuronal-migration-and-its-implications-in-cancer-cell-mobility
#10
REVIEW
Abiola A Ayanlaja, Ye Xiong, Yue Gao, GuangQuan Ji, Chuanxi Tang, Zamzam Abdikani Abdullah, DianShuai Gao
Neuronal migration is a critical process in the development of the nervous system. Defects in the migration of the neurons are associated with diseases like lissencephaly, subcortical band heterotopia (SBH), and pachygyria. Doublecortin (DCX) is an essential factor in neurogenesis and mutations in this protein impairs neuronal migration leading to several pathological conditions. Although, DCX is capable of modulating and stabilizing microtubules (MTs) to ensure effective migration, the mechanisms involved in executing these functions remain poorly understood...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28701916/the-role-of-hotair-mir-148b-3p-usf1-on-regulating-the-permeability-of-btb
#11
Libo Sa, Yan Li, Lini Zhao, Yunhui Liu, Ping Wang, Libo Liu, Zhen Li, Jun Ma, Heng Cai, Yixue Xue
Homeobox transcript antisense intergenic RNA (HOTAIR), as a long non-coding RNA (lncRNA), has been considered to play critical roles in the biological properties of various tumors. The purposes of this study were to investigate the role and possible molecular mechanisms of HOTAIR in regulating the permeability of blood tumor barrier (BTB) in vitro. Our present study elucidated that the expressions of HOTAIR and upstream stimulatory factor 1 (USF1) was up-regulated, but miR-148b-3p was down-regulated in glioma microvascular endothelial cells (GECs)...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28698714/corrigendum-adenosine-kinase-inhibition-protects-against-cranial-radiation-induced-cognitive-dysfunction
#12
Munjal M Acharya, Janet E Baulch, Theresa A Lusardi, Barrett D Allen, Nicole N Chmielewski, Al Anoud D Baddour, Charles L Limoli, Detlev Boison
[This corrects the article on p. 42 in vol. 9, PMID: 27375429.].
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28694771/nupr1-modulates-methamphetamine-induced-dopaminergic-neuronal-apoptosis-and-autophagy-through-chop-trib3-mediated-endoplasmic-reticulum-stress-signaling-pathway
#13
Xiang Xu, Enping Huang, Yunchun Tai, Xu Zhao, Xuebing Chen, Chuanxiang Chen, Rui Chen, Chao Liu, Zhoumeng Lin, Huijun Wang, Wei-Bing Xie
Methamphetamine (METH) is an illegal and widely abused psychoactive stimulant. METH exposure causes detrimental effects on multiple organ systems, primarily the nervous system, especially dopaminergic pathways, in both laboratory animals and humans. In this study, we hypothesized that Nuclear protein 1 (Nupr1/com1/p8) is involved in METH-induced neuronal apoptosis and autophagy through endoplasmic reticulum (ER) stress signaling pathway. To test this hypothesis, we measured the expression levels of Nupr1, ER stress protein markers CHOP and Trib3, apoptosis-related protein markers cleaved-caspase3 and PARP, as well as autophagy-related protein markers LC3 and Beclin-1 in brain tissues of adult male Sprague-Dawley (SD) rats, rat primary cultured neurons and the rat adrenal pheochromocytoma cells (PC12 cells) after METH exposure...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28690498/amyloid-precursor-like-proteins-aplp1-and-aplp2-are-dispensable-for-normal-development-of-the-neonatal-respiratory-network
#14
Kang Han, Ulrike C Müller, Swen Hülsmann
Recent studies using animal models indicated that the members of the amyloid precursor protein (APP) gene family are important for the formation, maintenance, and plasticity of synapses. Despite this, the specific role of the APP homologs APLP1 and APLP2 within the CNS and PNS is still poorly understood. In contrast to the subtle phenotypes of single mutants, double knockout mice (DKO) lacking APP/APLP2 or APLP1/APLP2 die within the first day after birth. Whereas APP/APLP2-DKO mice show severe deficits of neuromuscular morphology and transmission, the underlying cause of lethality of APLP1/APLP2-DKO mice remains unclear...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28680393/potential-value-of-genomic-copy-number-variations-in-schizophrenia
#15
REVIEW
Chuanjun Zhuo, Weihong Hou, Chongguang Lin, Lirong Hu, Jie Li
Schizophrenia is a devastating neuropsychiatric disorder affecting approximately 1% of the global population, and the disease has imposed a considerable burden on families and society. Although, the exact cause of schizophrenia remains unknown, several lines of scientific evidence have revealed that genetic variants are strongly correlated with the development and early onset of the disease. In fact, the heritability among patients suffering from schizophrenia is as high as 80%. Genomic copy number variations (CNVs) are one of the main forms of genomic variations, ubiquitously occurring in the human genome...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28680392/direct-anandamide-activation-of-trpv1-produces-divergent-calcium-and-current-responses
#16
Axel J Fenwick, Daniel K Fowler, Shaw-Wen Wu, Forrest J Shaffer, Jonathan E M Lindberg, Dallas C Kinch, James H Peters
In the brainstem nucleus of the solitary tract (NTS), primary vagal afferent neurons express the transient receptor potential vanilloid subfamily member 1 (TRPV1) at their central terminals where it contributes to quantal forms of glutamate release. The endogenous membrane lipid anandamide (AEA) is a putative TRPV1 agonist in the brain, yet the extent to which AEA activation of TRPV1 has a neurophysiological consequence is not well established. We investigated the ability of AEA to activate TRPV1 in vagal afferent neurons in comparison to capsaicin (CAP)...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28680391/the-role-of-the-multifunctional-bag3-protein-in-cellular-protein-quality-control-and-in-disease
#17
REVIEW
Elisabeth Stürner, Christian Behl
In neurons, but also in all other cells the complex proteostasis network is monitored and tightly regulated by the cellular protein quality control (PQC) system. Beyond folding of newly synthesized polypeptides and their refolding upon misfolding the PQC also manages the disposal of aberrant proteins either by the ubiquitin-proteasome machinery or by the autophagic-lysosomal system. Aggregated proteins are primarily degraded by a process termed selective macroautophagy (or aggrephagy). One such recently discovered selective macroautophagy pathway is mediated by the multifunctional HSP70 co-chaperone BAG3 (BCL-2-associated athanogene 3)...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28680390/the-role-of-the-heat-shock-protein-b8-hspb8-in-motoneuron-diseases
#18
REVIEW
Paola Rusmini, Riccardo Cristofani, Mariarita Galbiati, Maria E Cicardi, Marco Meroni, Veronica Ferrari, Giulia Vezzoli, Barbara Tedesco, Elio Messi, Margherita Piccolella, Serena Carra, Valeria Crippa, Angelo Poletti
Amyotrophic lateral sclerosis (ALS) and spinal and bulbar muscular atrophy (SBMA) are two motoneuron diseases (MNDs) characterized by aberrant protein behavior in affected cells. In familial ALS (fALS) and in SBMA specific gene mutations lead to the production of neurotoxic proteins or peptides prone to misfold, which then accumulate in form of aggregates. Notably, some of these proteins accumulate into aggregates also in sporadic ALS (sALS) even if not mutated. To prevent proteotoxic stresses detrimental to cells, misfolded and/or aggregated proteins must be rapidly removed by the protein quality control (PQC) system...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28676743/differential-alteration-in-expression-of-striatal-gabaar-subunits-in-mouse-models-of-huntington-s-disease
#19
Zhuowei Du, Margot Tertrais, Gilles Courtand, Thierry Leste-Lasserre, Laura Cardoit, Frédérique Masmejean, Christophe Halgand, Yoon H Cho, Maurice Garret
Huntington's disease (HD) is a neurodegenerative disorder characterized by progressive motor symptoms that are preceded by cognitive deficits and is considered as a disorder that primarily affects forebrain striatal neurons. To gain a better understanding of the molecular and cellular mechanisms associated with disease progression, we analyzed the expression of proteins involved in GABAergic neurotransmission in the striatum of the R6/1 transgenic mouse model. Western blot, quantitative PCR and immunohistochemical analyses were conducted on male R6/1 mice and age-matched wild type littermates...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28676742/complement-components-showed-a-time-dependent-local-expression-pattern-in-constant-and-acute-white-light-induced-photoreceptor-damage
#20
Nicole Schäfer, Antje Grosche, Sabrina I Schmitt, Barbara M Braunger, Diana Pauly
Background: Photoreceptor cell death due to extensive light exposure and induced oxidative-stress are associated with retinal degeneration. A correlated dysregulation of the complement system amplifies the damaging effects, but the local and time-dependent progression of this mechanism is not thoroughly understood. Methods: Light-induced photoreceptor damage (LD) was induced in Balb/c mice with white light illumination either for 24 h with 1000 lux (constant model) or 0.5 h with 5000 lux (acute model). Complement protein and mRNA expression levels were compared at 1 and 3 days post-LD for C1s, complement factor B (CFB), mannose binding lectin A, mannose-binding protein-associated serine protease 1 (MASP-1), C3, C4, C9, and complement factor P in retina and RPE/choroid...
2017: Frontiers in Molecular Neuroscience
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