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https://www.readbyqxmd.com/read/29660340/alteration-of-global-protein-sumoylation-in-neurons-and-astrocytes-in-response-to-alzheimer-s-disease-associated-insults
#1
Takuma Maruyama, Harmony Wada, Yoichiro Abe, Takako Niikura
SUMOylation, a post-translational modification of lysine residues by small ubiquitin-like modifier (SUMO) proteins, has been implicated in the pathogenesis of neurodegenerative disorders including Alzheimer's disease (AD), and in neuron- and astrocyte-specific physiological functions. Global SUMOylation is increased in the AD mouse brain in the pre-plaque-forming stage but returns to wild-type levels in the plaque-bearing stage. To clarify the reason for the transient change in SUMOylation, we analyzed the alteration of global SUMOylation induced by AD-associated cytotoxic stimuli in neurons and astrocytes individually...
June 2, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29530319/extranuclear-sumoylation-in-neurons
#2
REVIEW
Jeremy M Henley, Ruth E Carmichael, Kevin A Wilkinson
Post-translational modification of substrate proteins by SUMO conjugation regulates a diverse array of cellular processes. While predominantly a nuclear protein modification, there is a growing appreciation that SUMOylation of proteins outside the nucleus plays direct roles in controlling synaptic transmission, neuronal excitability, and adaptive responses to cell stress. Furthermore, alterations in protein SUMOylation are observed in a wide range of neurological and neurodegenerative diseases, and several extranuclear disease-associated proteins have been shown to be directly SUMOylated...
April 2018: Trends in Neurosciences
https://www.readbyqxmd.com/read/29472612/sumoylation-regulates-fmrp-mediated-dendritic-spine-elimination-and-maturation
#3
Anouar Khayachi, Carole Gwizdek, Gwénola Poupon, Damien Alcor, Magda Chafai, Frédéric Cassé, Thomas Maurin, Marta Prieto, Alessandra Folci, Fabienne De Graeve, Sara Castagnola, Romain Gautier, Lenka Schorova, Céline Loriol, Marie Pronot, Florence Besse, Frédéric Brau, Emmanuel Deval, Barbara Bardoni, Stéphane Martin
Fragile X syndrome (FXS) is the most frequent inherited cause of intellectual disability and the best-studied monogenic cause of autism. FXS results from the functional absence of the fragile X mental retardation protein (FMRP) leading to abnormal pruning and consequently to synaptic communication defects. Here we show that FMRP is a substrate of the small ubiquitin-like modifier (SUMO) pathway in the brain and identify its active SUMO sites. We unravel the functional consequences of FMRP sumoylation in neurons by combining molecular replacement strategy, biochemical reconstitution assays with advanced live-cell imaging...
February 22, 2018: Nature Communications
https://www.readbyqxmd.com/read/29277914/synaptic-localization-of-the-sumoylation-regulating-protease-senp5-in-the-adult-mouse-brain
#4
Hiroki Akiyama, Kazuhiko Nakadate, Shin-Ichi Sakakibara
Covalent conjugation of small ubiquitin-like modifiers (SUMOs) or SUMOylation is a reversible post-translational modification that regulates the stability and function of target proteins. SUMOs are removed from substrate proteins by sentrin/SUMO-specific proteases (SENPs). Numerous studies have implicated SUMOylation in various physiological and pathological processes in neurons. To understand the functional roles of SUMOylation, it is necessary to determine the distribution of enzymes regulating SUMO conjugation and deconjugation; yet, the localization of SENPs has not been described in detail in intact brain tissue...
April 15, 2018: Journal of Comparative Neurology
https://www.readbyqxmd.com/read/29180403/sumoylation-and-ubiquitination-reciprocally-regulate-%C3%AE-synuclein-degradation-and-pathological-aggregation
#5
Ruth Rott, Raymonde Szargel, Vered Shani, Haya Hamza, Mor Savyon, Fatimah Abd Elghani, Rina Bandopadhyay, Simone Engelender
α-Synuclein accumulation is a pathological hallmark of Parkinson's disease (PD). Ubiquitinated α-synuclein is targeted to proteasomal or lysosomal degradation. Here, we identify SUMOylation as a major mechanism that counteracts ubiquitination by different E3 ubiquitin ligases and regulates α-synuclein degradation. We report that PIAS2 promotes SUMOylation of α-synuclein, leading to a decrease in α-synuclein ubiquitination by SIAH and Nedd4 ubiquitin ligases, and causing its accumulation and aggregation into inclusions...
December 12, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29098326/sumoylation-controls-stem-cell-proliferation-and-regional-cell-death-through-hedgehog-signaling-in-planarians
#6
Manish Thiruvalluvan, Paul G Barghouth, Assaf Tsur, Limor Broday, Néstor J Oviedo
Mechanisms underlying anteroposterior body axis differences during adult tissue maintenance and regeneration are poorly understood. Here, we identify that post-translational modifications through the SUMO (Small Ubiquitin-like Modifier) machinery are evolutionarily conserved in the Lophotrocozoan Schmidtea mediterranea. Disruption of SUMOylation in adult animals by RNA-interference of the only SUMO E2 conjugating enzyme Ubc9 leads to a systemic increase in DNA damage and a remarkable regional defect characterized by increased cell death and loss of the posterior half of the body...
April 2018: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/29058184/hyper-sumoylation-of-k-channels-in-sudden-unexplained-death-in-epilepsy-isolation-and-primary-culture-of-dissociated-hippocampal-neurons-from-newborn-mice-for-subcellular-localization
#7
Xu Chen, Shanshan Zhang, Jifang Huang, Wanying Dong, Hui Xiao, Huanjie Shao, Jinke Cheng, Hongmei Wu, Yitao Qi
The physiological characteristics of rat and murine hippocampal neurons are widely studied, especially because of the involvement of the hippocampus in learning, memory, and neurological functions. Primary cultures of hippocampal neurons are commonly used to discover cellular and molecular mechanisms in neurobiology. By isolating and culturing individual hippocampal neurons, neuroscientists are able to investigate the activity of neurons at the individual cell and single synapse level, and to analyze properties related to cellular structure, cellular trafficking, and individual protein subcellular localization or protein-protein interaction using a variety of biochemical techniques...
2018: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28713906/chronic-administration-of-sumo%C3%A2-1-has-negative-effects-on-novel-object-recognition-memory-as-well-as-cell-proliferation-and-neuroblast-differentiation-in-the-mouse-dentate-gyrus
#8
Dae Young Yoo, Dae Won Kim, Hyun Jung Kwon, Hyo Young Jung, Sung Min Nam, Jong Whi Kim, Jin Young Chung, Moo-Ho Won, Yeo Sung Yoon, Soo Young Choi, In Koo Hwang
Post‑translational modifications have been associated with developmental and aging processes, as well as in the pathogenesis of certain diseases. The present study aimed to investigate the effects of small ubiquitin‑like modifier 1 (SUMO‑1) on hippocampal dependent memory function, cell proliferation and neuroblast differentiation. To facilitate the delivery of SUMO‑1 into hippocampal neurons, a transactivator of transcription (Tat)‑SUMO‑1 fusion protein was constructed and mice were divided into two groups: A vehicle (Tat peptide)‑treated group and a Tat‑SUMO‑1‑treated group...
September 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28713891/hypothermia-exerts-early-neuroprotective-effects-involving-protein-conjugation-of-sumo%C3%A2-2-3-in-a-rat-model-of-middle-cerebral-artery-occlusion
#9
Gang Li, Xiaozhi Liu, Zhiguo Su, Dong Zhang
How hypothermia serves an early protective role against cerebral ischemia remains to be determined. The small ubiquitin‑related modifier protein (SUMO) functions as a post‑translational modification system and SUMO‑2/3 subtypes are often activated in early stress. The present study investigated changes in the protein level of SUMO using western blotting and immunocytochemistry when neurons were exposed to oxygen‑glucose deprivation (OGD) in vitro, as well as in a rat model of middle cerebral artery occlusion (MCAO) in vivo...
September 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28598330/analysis-of-sumo1-conjugation-at-synapses
#10
James A Daniel, Benjamin H Cooper, Jorma J Palvimo, Fu-Ping Zhang, Nils Brose, Marilyn Tirard
SUMO1-conjugation of proteins at neuronal synapses is considered to be a major post-translational regulatory process in nerve cell and synapse function, but the published evidence for SUMO1-conjugation at synapses is contradictory. We employed multiple genetic mouse models for stringently controlled biochemical and immunostaining analyses of synaptic SUMO1-conjugation. By using a knock-in reporter mouse line expressing tagged SUMO1, we could not detect SUMO1-conjugation of seven previously proposed synaptic SUMO1-targets in the brain...
June 9, 2017: ELife
https://www.readbyqxmd.com/read/28501776/inhibition-of-senp3-by-urb597-ameliorates-neurovascular-unit-dysfunction-in-rats-with-chronic-cerebral-hypoperfusion
#11
Da-Peng Wang, Ke-Jia Liu, Graham Kasper, Qi Lin, Jian Hai
Disruption of the neurovascular unit (NVU), induced by chronic cerebral hypoperfusion (CCH), has been broadly found in various neurological disorders. SUMO-specific protease 3 (SENP3) is expressed in neurons, astrocytes, and microglia, and regulates a variety of cell events. However, whether SENP3 is involved in neurovascular injury under the condition of CCH is still elusive. To address this issue, we investigated the effect of the fatty acid amide hydrolase (FAAH) inhibitor URB597 on NVU and the role of SENP3 in this process, as well as the underling mechanisms...
July 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28487986/sumo-1-delays-neuronal-damage-in-the-spinal-cord-following-ischemia-reperfusion
#12
Hyo Young Jung, Dae Won Kim, Hyun Jung Kwon, Dae Young Yoo, In Koo Hwang, Moo-Ho Won, Tack-Geun Cho, Soo Young Choi, Seung Myung Moon
The present study investigated the protective effects of small ubiquitin-like modifier 1 (SUMO-1) on spinal cord ischemic damage in rabbits. A trans‑activator of transcription (Tat)‑SUMO‑1 fusion protein was prepared, and transient spinal cord ischemia was induced by occlusion of the abdominal aorta for 15 min. Vehicle (glycerol) or 1 mg/kg Tat-1-SUMO‑1 was administered intraperitoneally to the rabbits immediately following ischemia/reperfusion. Administration of Tat-SUMO-1 did not lead to significant alterations in arterial blood gases [partial pressure (Pa)CO2 and PaO2], pH, or blood glucose levels prior to ischemia, 10 min after occlusion or 10 min after reperfusion...
June 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28323006/the-role-of-sumoylation-in-cerebral-hypoxia-and-ischemia
#13
REVIEW
Myriam Peters, Betty Wielsch, Johannes Boltze
The process of protein modification by adding or detaching small ubiquitin-like modifiers (SUMO) proteins, called SUMOylation, contributes to the regulation of numerous processes in eukaryotic cells. SUMOylation also represents a key response and adaption mechanism to different forms of metabolic stress. The central nervous system (CNS) and neurons in particular are highly susceptible to hypoxic-ischemic stress due to the lack of significant oxygen and energy reserves. SUMOylation is observed in many molecular responses to metabolic stress in the brain, and is therefore supposed to represent an endogenous neuroprotective mechanism...
July 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28277940/a-single-structurally-conserved-sumoylation-site-in-crmp2-controls-nav1-7-function
#14
Erik Thomas Dustrude, Samantha Perez-Miller, Liberty François-Moutal, Aubin Moutal, May Khanna, Rajesh Khanna
The neuronal collapsin response mediator protein 2 (CRMP2) undergoes several posttranslational modifications that codify its functions. Most recently, CRMP2 SUMOylation (addition of small ubiquitin like modifier (SUMO)) was identified as a key regulatory step within a modification program that codes for CRMP2 interaction with, and trafficking of, voltage-gated sodium channel NaV1.7. In this paper, we illustrate the utility of combining sequence alignment within protein families with structural analysis to identify, from several putative SUMOylation sites, those that are most likely to be biologically relevant...
July 4, 2017: Channels
https://www.readbyqxmd.com/read/28197918/sumoylation-implications-for-neurodegenerative-diseases
#15
REVIEW
Dina B Anderson, Camila A Zanella, Jeremy M Henley, Helena Cimarosti
The covalent posttranslational modifications of proteins are critical events in signaling cascades that enable cells to efficiently, rapidly and reversibly respond to extracellular stimuli. This is especially important in the CNS where the processes affecting synaptic communication between neurons are highly complex and very tightly regulated. Sumoylation regulates the function and fate of a diverse array of proteins and participates in the complex cell signaling pathways required for cell survival. One of the most complex signaling pathways is synaptic transmission...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28197910/sumo-modification-of-ion-channels
#16
REVIEW
Mark Benson, Jorge A Iñiguez-Lluhí, Jeffrey Martens
Recently, a role for SUMO modification outside of the nucleus has emerged. Although the number of extranuclear proteins known to be sumoylated is comparatively small, ion channels represent one important new class of these proteins. Ion channels are responsible for the control of membrane excitability and therefore are critical for fundamental physiological processes such as muscle contraction, neuronal firing, and cellular homeostasis. As such, these ion-conducting proteins are subject to precise regulation...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28186506/epigenetic-regulation-of-hdac1-sumoylation-as-an-endogenous-neuroprotection-against-a%C3%AE-toxicity-in-a-mouse-model-of-alzheimer-s-disease
#17
Chih Chieh Tao, Wei Lun Hsu, Yun Li Ma, Sin Jhong Cheng, Eminy Hy Lee
Amyloid-β (Aβ) produces neurotoxicity in the brain and causes neuronal death, but the endogenous defense mechanism that is activated on Aβ insult is less well known. Here we found that acute Aβ increases the expression of PIAS1 and Mcl-1 via activation of MAPK/ERK, and Aβ induction of PIAS1 enhances HDAC1 SUMOylation in rat hippocampus. Knockdown of PIAS1 decreases endogenous HDAC1 SUMOylation and blocks Aβ induction of Mcl-1. Sumoylated HDAC1 reduces it association with CREB, increases CREB binding to the Mcl-1 promoter and mediates Aβ induction of Mcl-1 expression...
April 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28067168/sumoylation-in-neurological-diseases
#18
F-Y Liu, Y-F Liu, Y Yang, Z-W Luo, J-W Xiang, Z-G Chen, R-L Qi, T-H Yang, Y Xiao, W-J Qing, D W-C Li
Since the discovery of SUMOs (small ubiquitin-like modifiers) over 20 years ago, sumoylation has recently emerged as an important posttranslational modification involved in almost all aspects of cellular physiology. In neurons, sumoylation dynamically modulates protein function and consequently plays an important role in neuronal maturation, synapse formation and plasticity. Thus, the dysfunction of sumoylation pathway is associated with many different neurological disorders. Hundreds of different proteins implicated in the pathogenesis of neurological disorders are SUMO-modified, indicating the importance of sumoylation involved in the neurological diseases...
2017: Current Molecular Medicine
https://www.readbyqxmd.com/read/28029095/sumoylation-of-nav1-2-channels-mediates-the-early-response-to-acute-hypoxia-in-central-neurons
#19
Leigh D Plant, Jeremy D Marks, Steve An Goldstein
The mechanism for the earliest response of central neurons to hypoxia-an increase in voltage-gated sodium current (INa)-has been unknown. Here, we show that hypoxia activates the Small Ubiquitin-like Modifier (SUMO) pathway in rat cerebellar granule neurons (CGN) and that SUMOylation of NaV1.2 channels increases INa. The time-course for SUMOylation of single NaV1.2 channels at the cell surface and changes in INa coincide, and both are prevented by mutation of NaV1.2-Lys38 or application of a deSUMOylating enzyme...
December 28, 2016: ELife
https://www.readbyqxmd.com/read/27986376/bilateral-upregulation-of-%C3%AE-synuclein-expression-in-the-mouse-substantia-nigra-by-intracranial-rotenone-treatment
#20
Candace H Carriere, Na Hyea Kang, Lennard P Niles
The pesticide rotenone has been shown to cause systemic inhibition of mitochondrial complex I activity, with consequent degeneration of dopamine neurons along the nigrostriatal pathway, as observed in Parkinson's disease (PD). Recently, intracranial infusion of rotenone was found to increase the protein levels of the Lewy body constituents, α-synuclein and small ubiquitin-related modifier-1(SUMO-1), in the lesioned hemisphere of the mouse brain. These findings are supportive of a mouse model of PD, but information about the dopamine-synthesizing enzyme, tyrosine hydroxylase (TH), an essential marker of dopaminergic status, was not reported...
February 2017: Experimental and Toxicologic Pathology: Official Journal of the Gesellschaft Für Toxikologische Pathologie
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