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https://www.readbyqxmd.com/read/28943839/cellular-chaperones-as-therapeutic-targets-in-als-to-restore-protein-homeostasis-and-improve-cellular-function
#1
REVIEW
Bernadett Kalmar, Linda Greensmith
Heat shock proteins (Hsps) are ubiquitously expressed chaperone proteins that enable cells to cope with environmental stresses that cause misfolding and denaturation of proteins. With aging this protein quality control machinery becomes less effective, reducing the ability of cells to cope with damaging environmental stresses and disease-causing mutations. In neurodegenerative disorders such as Amyotrophic Lateral Sclerosis (ALS), such mutations are known to result in protein misfolding, which in turn results in the formation of intracellular aggregates cellular dysfunction and eventual neuronal death...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28943283/step-inhibition-reverses-behavioral-electrophysiologic-and-synaptic-abnormalities-in-fmr1-ko-mice
#2
Manavi Chatterjee, Pradeep K Kurup, Camilla J Lundbye, Anna Karina Hugger Toft, Jeemin Kwon, Jessie Benedict, Marija Kamceva, Tue G Banke, Paul J Lombroso
Fragile X syndrome (FXS) is the leading cause of inherited intellectual disability, with additional symptoms including attention deficit and hyperactivity, anxiety, impulsivity, and repetitive movements or actions. The majority of FXS cases are attributed to a CGG expansion that leads to transcriptional silencing and diminished expression of fragile X mental retardation protein (FMRP). FMRP, an RNA binding protein, regulates the synthesis of dendritically-translated mRNAs by stalling ribosomal translation. Loss of FMRP leads to increased translation of some of these mRNAs, including the CNS-specific tyrosine phosphatase STEP (STriatal-Enriched protein tyrosine Phosphatase)...
September 21, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28941008/non-canonical-bases-in-the-genome-the-regulatory-information-layer-in-dna
#3
Thomas Carell, Matthias Q Kurz, Markus Müller, Martin Rossa, Fabio Spada
The sequence of the four canonical bases dA, dC, dG and dT forming two defined Watson-Crick base pairs (dT:dA, dG:dC), held together by H-bonding, establish the sequence information in the DNA double strand. The faithful replication of the sequence information during cell division, the transcription of the DNA information into RNA and the final translation of the sequence information into proteins is the basis for life on earth. Multicellular organisms developed the concept of specialized cells that perform specific functions...
September 21, 2017: Angewandte Chemie
https://www.readbyqxmd.com/read/28939666/the-e2a-splice-variant-e47-regulates-the-differentiation-of-projection-neurons-via-p57-kip2-during-cortical-development
#4
Sabrina Pfurr, Yu-Hsuan Chu, Christian Bohrer, Franziska Greulich, Robert Beattie, Könül Mammadzada, Miriam Hils, Sebastian J Arnold, Verdon Taylor, Kristina Schachtrup, N Henriette Uhlenhaut, Christian Schachtrup
During corticogenesis, distinct classes of neurons are born from progenitor cells located in the ventricular and subventricular zones, from where they migrate towards the pial surface to assemble into highly organized layer-specific circuits. However, the precise and coordinated transcriptional network activity defining neuronal identity is still not understood. Here, we show that genetic depletion of the basic helix-loop-helix (bHLH) transcription factor E2A splice variant E47 increased the number of Tbr1-positive deep layer and Satb2-positive upper layer neurons at E14...
September 22, 2017: Development
https://www.readbyqxmd.com/read/28938481/vesicular-glutamate-transporter-1-knockdown-in-infralimbic-prefrontal-cortex-augments-neuroendocrine-responses-to-chronic-stress-in-male-rats
#5
Brent Myers, Jessica M McKlveen, Rachel Morano, Yvonne M Ulrich-Lai, Matia B Solomon, Steven P Wilson, James P Herman
Chronic stress-associated pathologies frequently associate with alterations in the structure and activity of medial prefrontal cortex (mPFC). However, the influence of infralimbic cortex (IL) projection neurons on HPA axis activity is unknown, as is the involvement of these cells in chronic stress-induced endocrine alterations. In the current study, a lentiviral-packaged vector coding for a small interfering RNA (siRNA) targeting vesicular glutamate transporter 1 (vGluT1) mRNA was microinjected into the IL of male rats...
July 25, 2017: Endocrinology
https://www.readbyqxmd.com/read/28936781/coordinate-expression-of-pan-neuronal-and-functional-signature-genes-in-sympathetic-neurons
#6
U Ernsberger, M Kramer, K Tsarovina, T Deller, H Rohrer
Neuron subtypes of the mature nervous system differ in the expression of characteristic marker genes while they share the expression of generic neuronal genes. The regulatory logic that maintains subtype-specific and pan-neuronal genes is not well understood. To begin to address this issue, we analyze RNA sequencing results from whole sympathetic ganglia and single sympathetic neurons in the mouse. We focus on gene products involved in the neuronal cytoskeleton, neurotransmitter synthesis and storage, transmitter release and reception and electrical information processing...
September 21, 2017: Cell and Tissue Research
https://www.readbyqxmd.com/read/28936164/sodium-arsenite-induced-learning-and-memory-impairment-is-associated-with-endoplasmic-reticulum-stress-mediated-apoptosis-in-rat-hippocampus
#7
Hongna Sun, Yanmei Yang, Hanwen Shao, Weiwei Sun, Muyu Gu, Hui Wang, Lixin Jiang, Lisha Qu, Dianjun Sun, Yanhui Gao
Chronic arsenic exposure has been associated to cognitive deficits. However, mechanisms remain unknown. The present study investigated the neurotoxic effects of sodium arsenite in drinking water over different dosages and time periods. Based on results from the Morris water maze (MWM) and morphological analysis, an exposure to sodium arsenite could induce neuronal damage in the hippocampus, reduce learning ability, and accelerate memory impairment. Sodium arsenite significantly increased homocysteine levels in serum and brain...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28936162/rna-sequencing-analysis-reveals-a-regulatory-role-for-transcription-factor-fezf2-in-the-mature-motor-cortex
#8
Alison J Clare, Hollie E Wicky, Ruth M Empson, Stephanie M Hughes
Forebrain embryonic zinc finger (Fezf2) encodes a transcription factor essential for the specification of layer 5 projection neurons (PNs) in the developing cerebral cortex. As with many developmental transcription factors, Fezf2 continues to be expressed into adulthood, suggesting it remains crucial to the maintenance of neuronal phenotypes. Despite the continued expression, a function has yet to be explored for Fezf2 in the PNs of the developed cortex. Here, we investigated the role of Fezf2 in mature neurons, using lentiviral-mediated delivery of a shRNA to conditionally knockdown the expression of Fezf2 in the mouse primary motor cortex (M1)...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28934222/endogenous-rgs14-is-a-cytoplasmic-nuclear-shuttling-protein-that-localizes-to-juxtanuclear-membranes-and-chromatin-rich-regions-of-the-nucleus
#9
Mary Rose Branch, John R Hepler
Regulator of G protein signaling 14 (RGS14) is a multifunctional scaffolding protein that integrates G protein and H-Ras/MAPkinase signaling pathways to regulate synaptic plasticity important for hippocampal learning and memory. However, to date, little is known about the subcellular distribution and roles of endogenous RGS14 in a neuronal cell line. Most of what is known about RGS14 cellular behavior is based on studies of tagged, recombinant RGS14 ectopically overexpressed in unnatural host cells. Here, we report for the first time a comprehensive assessment of the subcellular distribution and dynamic localization of endogenous RGS14 in rat B35 neuroblastoma cells...
2017: PloS One
https://www.readbyqxmd.com/read/28933219/suppression-of-trim32-enhances-motor-function-repair-after-traumatic-brain-injury-associated-with-antiapoptosis
#10
Zi-Bin Zhang, Liu-Lin Xiong, Bin-Tuan Lu, Hui-Xiang Zhang, Piao Zhang, Ting-Hua Wang
To investigate the role of Trim32 in traumatic brain injury (TBI), adult male Sprague Dawley (SD) rats and mice were randomly divided into sham (n = 6) and TBI groups ( n = 24), respectively. Then, mice were assigned into Trim32 knockout mice (Trim32-KO [+/-]) and wild-type (WT) littermates. The TBI model used was the Feeney free-falling model, and neurological function was evaluated after TBI using a neurological severity score (NSS). Reverse transcription polymerase chain reaction (RT-PCR), Western blot, and immunohistochemistry were used to investigate the expression of Trim32 in the damaged cortex...
July 2017: Cell Transplantation
https://www.readbyqxmd.com/read/28931688/a-selective-bottleneck-shapes-the-evolutionary-mutant-spectra-of-enterovirus-a71-during-viral-dissemination-in-humans
#11
Sheng-Wen Huang, Yi-Hui Huang, Huey-Pin Tsai, Pin-Hwa Kuo, Shih-Min Wang, Ching-Chuan Liu, Jen-Ren Wang
RNA viruses accumulate mutations to rapidly adapt to environmental changes. Enterovirus A71 (EV-A71) causes various clinical manifestations with occasional severe neurological complications. However, the mechanism by which EV-A71 evolves within the human body is unclear. Utilizing deep sequencing and haplotype analyses of viruses from various tissues of an autopsy patient, we sought to define the evolutionary pathway by which enterovirus A71 evolves fitness for invading the central nervous system in humans...
September 20, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28930607/transcriptomics-in-amyotrophic-lateral-sclerosis
#12
Marios G Krokidis, Panagiotis Vlamos
Amyotrophic lateral sclerosis (ALS) is an adult-onset, incurable neurodegenerative disease characterized by the selective death of upper and lowers motor neurons in the spinal cord, brainstem and motor cortex, which ultimately leads to paralysis and death within 2-3 years of onset. ALS is poorly understood, although multiple studies have been proposed to explain the pathophysiological mechanisms of the disorder. The development of microarray technology, for simultaneous analysis of the transcriptional expression of thousands of genes, has provided new possibilities to get better insights into the pathogenesis of ALS, and most important, potential new candidate targets for novel treatments...
January 1, 2018: Frontiers in Bioscience (Elite Edition)
https://www.readbyqxmd.com/read/28929094/gestational-age-dependent-increase-of-survival-motor-neuron-protein-in-umbilical-cord-derived-mesenchymal-stem-cells
#13
Sota Iwatani, Nur Imma Fatimah Harahap, Dian Kesumapramudya Nurputra, Shinya Tairaku, Akemi Shono, Daisuke Kurokawa, Keiji Yamana, Khin Kyae Mon Thwin, Makiko Yoshida, Masami Mizobuchi, Tsubasa Koda, Kazumichi Fujioka, Mariko Taniguchi-Ikeda, Hideto Yamada, Ichiro Morioka, Kazumoto Iijima, Hisahide Nishio, Noriyuki Nishimura
BACKGROUND: Spinal muscular atrophy (SMA) is the most common genetic neurological disease leading to infant death. It is caused by loss of survival motor neuron (SMN) 1 gene and subsequent reduction of SMN protein in motor neurons. Because SMN is ubiquitously expressed and functionally linked to general RNA metabolism pathway, fibroblasts (FBs) are most widely used for the assessment of SMN expression in SMA patients but usually isolated from skin biopsy samples after the onset of overt symptoms...
2017: Frontiers in Pediatrics
https://www.readbyqxmd.com/read/28928394/rna-localization-is-a-key-determinant-of-neurite-enriched-proteome
#14
Alessandra Zappulo, David van den Bruck, Camilla Ciolli Mattioli, Vedran Franke, Koshi Imami, Erik McShane, Mireia Moreno-Estelles, Lorenzo Calviello, Andrei Filipchyk, Esteban Peguero-Sanchez, Thomas Müller, Andrew Woehler, Carmen Birchmeier, Enrique Merino, Nikolaus Rajewsky, Uwe Ohler, Esteban O Mazzoni, Matthias Selbach, Altuna Akalin, Marina Chekulaeva
Protein subcellular localization is fundamental to the establishment of the body axis, cell migration, synaptic plasticity, and a vast range of other biological processes. Protein localization occurs through three mechanisms: protein transport, mRNA localization, and local translation. However, the relative contribution of each process to neuronal polarity remains unknown. Using neurons differentiated from mouse embryonic stem cells, we analyze protein and RNA expression and translation rates in isolated cell bodies and neurites genome-wide...
September 19, 2017: Nature Communications
https://www.readbyqxmd.com/read/28925356/the-c-elegans-neural-editome-reveals-an-adar-target-mrna-required-for-proper-chemotaxis
#15
Sarah N Deffit, Brian A Yee, Aidan C Manning, Suba Rajendren, Pranathi Vadlamani, Emily C Wheeler, Alain Domissy, Michael C Washburn, Gene W Yeo, Heather A Hundley
ADAR proteins alter gene expression both by catalyzing adenosine (A) to inosine (I) RNA editing and binding to regulatory elements in target RNAs. Loss of ADARs affects neuronal function in all animals studied to date. Caenorhabditis elegans lacking ADARs exhibit reduced chemotaxis, but the targets responsible for this phenotype remain unknown. To identify critical neural ADAR targets in C. elegans, we performed an unbiased assessment of the effects of ADR-2, the only A-to-I editing enzyme in C. elegans, on the neural transcriptome...
September 19, 2017: ELife
https://www.readbyqxmd.com/read/28924186/interactome-analysis-reveals-znf804a-a-schizophrenia-risk-gene-as-a-novel-component-of-protein-translational-machinery-critical-for-embryonic-neurodevelopment
#16
Y Zhou, F Dong, T A Lanz, V Reinhart, M Li, L Liu, J Zou, H S Xi, Y Mao
Recent genome-wide association studies identified over 100 genetic loci that significantly associate with schizophrenia (SZ). A top candidate gene, ZNF804A, was robustly replicated in different populations. However, its neural functions are largely unknown. Here we show in mouse that ZFP804A, the homolog of ZNF804A, is required for normal progenitor proliferation and neuronal migration. Using a yeast two-hybrid genome-wide screen, we identified novel interacting proteins of ZNF804A. Rather than transcriptional factors, genes involved in mRNA translation are highly represented in our interactome result...
September 19, 2017: Molecular Psychiatry
https://www.readbyqxmd.com/read/28923083/prevention-of-c5ar1-signaling-delays-microglial-inflammatory-polarization-favors-clearance-pathways-and-suppresses-cognitive-loss
#17
Michael X Hernandez, Shan Jiang, Tracy A Cole, Shu-Hui Chu, Maria I Fonseca, Melody J Fang, Lindsay A Hohsfield, Maria D Torres, Kim N Green, Rick A Wetsel, Ali Mortazavi, Andrea J Tenner
BACKGROUND: Pharmacologic inhibition of C5aR1, a receptor for the complement activation proinflammatory fragment, C5a, suppressed pathology and cognitive deficits in Alzheimer's disease (AD) mouse models. To validate that the effect of the antagonist was specifically via C5aR1 inhibition, mice lacking C5aR1 were generated and compared in behavior and pathology. In addition, since C5aR1 is primarily expressed on cells of the myeloid lineage, and only to a lesser extent on endothelial cells and neurons in brain, gene expression in microglia isolated from adult brain at multiple ages was compared across all genotypes...
September 18, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28920956/biotin-tagging-of-mecp2-in-mice-reveals-contextual-insights-into-the-rett-syndrome-transcriptome
#18
Brian S Johnson, Ying-Tao Zhao, Maria Fasolino, Janine M Lamonica, Yoon Jung Kim, George Georgakilas, Kathleen H Wood, Daniel Bu, Yue Cui, Darren Goffin, Golnaz Vahedi, Tae Hoon Kim, Zhaolan Zhou
Mutations in MECP2 cause Rett syndrome (RTT), an X-linked neurological disorder characterized by regressive loss of neurodevelopmental milestones and acquired psychomotor deficits. However, the cellular heterogeneity of the brain impedes an understanding of how MECP2 mutations contribute to RTT. Here we developed a Cre-inducible method for cell-type-specific biotin tagging of MeCP2 in mice. Combining this approach with an allelic series of knock-in mice carrying frequent RTT-associated mutations (encoding T158M and R106W) enabled the selective profiling of RTT-associated nuclear transcriptomes in excitatory and inhibitory cortical neurons...
September 18, 2017: Nature Medicine
https://www.readbyqxmd.com/read/28918081/developmental-alcohol-exposure-impairs-synaptic-plasticity-without-overtly-altering-microglial-function-in-mouse-visual-cortex
#19
Elissa L Wong, Nina M Lutz, Victoria A Hogan, Cassandra E Lamantia, Helene R McMurray, Jason R Myers, John M Ashton, Ania K Majewska
Fetal alcohol spectrum disorder (FASD), caused by gestational ethanol (EtOH) exposure, is one of the most common causes of non-heritable and life-long mental disability worldwide, with no standard treatment or therapy available. While EtOH exposure can alter the function of both neurons and glia, it is still unclear how EtOH influences brain development to cause deficits in sensory and cognitive processing later in life. Microglia play an important role in shaping synaptic function and plasticity during neural circuit development and have been shown to mount an acute immunological response to EtOH exposure in certain brain regions...
September 13, 2017: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/28918022/antisense-oligonucleotides-reduce-rna-foci-in-spinocerebellar-ataxia-36-patient-ipscs
#20
Kosuke Matsuzono, Keiko Imamura, Nagahisa Murakami, Kayoko Tsukita, Takuya Yamamoto, Yuishin Izumi, Ryuji Kaji, Yasuyuki Ohta, Toru Yamashita, Koji Abe, Haruhisa Inoue
Spinocerebellar ataxia type 36 is a late-onset, slowly progressive cerebellar syndrome with motor neuron degeneration that is caused by expansions of a hexanucleotide repeat (GGCCTG) in the noncoding region of NOP56 gene, with a histopathological feature of RNA foci formation in postmortem tissues. Here, we report a cellular model using the spinocerebellar ataxia type 36 patient induced pluripotent stem cells (iPSCs). We generated iPSCs from spinocerebellar ataxia type 36 patients and differentiated them into neurons...
September 15, 2017: Molecular Therapy. Nucleic Acids
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