keyword
MENU ▼
Read by QxMD icon Read
search

sumo neuron

keyword
https://www.readbyqxmd.com/read/28323006/the-role-of-sumoylation-in-cerebral-hypoxia-and-ischemia
#1
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...
March 17, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28277940/a-single-structurally-conserved-sumoylation-site-in-crmp2-controls-nav1-7-function
#2
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...
February 28, 2017: Channels
https://www.readbyqxmd.com/read/28197918/sumoylation-implications-for-neurodegenerative-diseases
#3
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
#4
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
#5
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
#6
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 post-translational 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...
January 9, 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
#7
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
#8
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
https://www.readbyqxmd.com/read/27940916/hierarchical-crmp2-posttranslational-modifications-control-nav1-7-function
#9
Erik T Dustrude, Aubin Moutal, Xiaofang Yang, Yuying Wang, May Khanna, Rajesh Khanna
Voltage-gated sodium channels are crucial determinants of neuronal excitability and signaling. Trafficking of the voltage-gated sodium channel NaV1.7 is dysregulated in neuropathic pain. We identify a trafficking program for NaV1.7 driven by hierarchical interactions with posttranslationally modified versions of the binding partner collapsin response mediator protein 2 (CRMP2). The binding described between CRMP2 and NaV1.7 was enhanced by conjugation of CRMP2 with small ubiquitin-like modifier (SUMO) and further controlled by the phosphorylation status of CRMP2...
December 27, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27919694/neuron-specific-sumo-knockdown-suppresses-global-gene-expression-response-and-worsens-functional-outcome-after-transient-forebrain-ischemia-in-mice
#10
Lin Zhang, Xiaozhi Liu, Huaxin Sheng, Shuai Liu, Ying Li, Julia Q Zhao, David S Warner, Wulf Paschen, Wei Yang
Small ubiquitin-like modifier (SUMO) conjugation (SUMOylation) plays key roles in neurologic function in health and disease. Neuronal SUMOylation is essential for emotionality and cognition, and this pathway is dramatically activated in post-ischemic neurons, a neuroprotective response to ischemia. It is also known from cell culture studies that SUMOylation modulates gene expression. However, it remains unknown how SUMOylation regulates neuronal gene expression in vivo, in the physiologic state and after ischemia, and modulates post-ischemic recovery of neurologic function...
February 20, 2017: Neuroscience
https://www.readbyqxmd.com/read/27882949/sumo-specific-protease-1-protects-neurons-from-apoptotic-death-during-transient-brain-ischemia-reperfusion
#11
Huijun Zhang, Yan Wang, Aoxue Zhu, Dehua Huang, Shining Deng, Jinke Cheng, Michael X Zhu, Yong Li
SUMO-specific protease 1 (SENP1) deconjugates SUMO from modified proteins. Although post-ischemic activation of SUMO conjugation was suggested to be neuroprotective against ischemia/reperfusion (I/R) injury, the function of SENP1 in this process remained unclear. Here we show that transient middle cerebral artery occlusion in mice followed by 6, 12 and 24 h reperfusion significantly enhanced SENP1 levels in the affected brain area, independent of transcription. Consistent with the increase in SENP1, the levels of SUMO1-conjugated proteins were decreased by I/R in cortical neurons of control littermate mice, but unchanged in that of animals with conditional ablation of SENP1 gene from adult principal neurons, the SENP1(flox/flox):CamKIIα-Cre (SENP1 cKO) mice...
November 24, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27819299/several-posttranslational-modifications-act-in-concert-to-regulate-gephyrin-scaffolding-and-gabaergic-transmission
#12
Himanish Ghosh, Luca Auguadri, Sereina Battaglia, Zahra Simone Thirouin, Khaled Zemoura, Simon Messner, Mario A Acuña, Hendrik Wildner, Gonzalo E Yévenes, Andrea Dieter, Hiroshi Kawasaki, Michael O Hottiger, Hanns Ulrich Zeilhofer, Jean-Marc Fritschy, Shiva K Tyagarajan
GABAA receptors (GABAARs) mediate the majority of fast inhibitory neurotransmission in the brain via synergistic association with the postsynaptic scaffolding protein gephyrin and its interaction partners. However, unlike their counterparts at glutamatergic synapses, gephyrin and its binding partners lack canonical protein interaction motifs; hence, the molecular basis for gephyrin scaffolding has remained unclear. In this study, we identify and characterize two new posttranslational modifications of gephyrin, SUMOylation and acetylation...
November 7, 2016: Nature Communications
https://www.readbyqxmd.com/read/27747316/tyrosyl-dna-phosphodiesterase-i-a-critical-survival-factor-for-neuronal-development-and-homeostasis
#13
Robert C A M van Waardenburg
Tyrosyl-DNA phosphodiesterase I (TDP1), like most DNA repair associated proteins, is not essential for cell viability. However, dysfunctioning TDP1 or ATM (ataxia telangiectasia mutated) results in autosomal recessive neuropathology with similar phenotypes, including cerebellar atrophy. Dual inactivation of TDP1 and ATM causes synthetic lethality. A TDP1H(493)R catalytic mutant is associated with spinocerebellar ataxia with axonal neuropathy (SCAN1), and stabilizes the TDP1 catalytic obligatory enzyme-DNA covalent complex...
2016: Journal of Neurology & Neuromedicine
https://www.readbyqxmd.com/read/27717094/terminal-differentiation-of-cortical-neurons-rapidly-remodels-rangap-mediated-nuclear-transport-system
#14
Kazushiro Fujiwara, Koichi Hasegawa, Masahiro Oka, Yoshihiro Yoneda, Kazuaki Yoshikawa
Terminal differentiation of neurons is accompanied by irreversible exit from the cell cycle and expression of neuronal phenotypes. The molecular mechanism whereby committed neuronal progenitors lose their ability to reenter the cell cycle is largely unknown. Here, we report that the nuclear transport system is rapidly remodeled in primary cortical progenitor cells (CPCs) at the very beginning of neuronal terminal differentiation. High levels of Ran GTPase-activating protein 1 (RanGAP), a key regulator of the Ran GTP-GDP cycle, in primary CPCs are drastically reduced upon neuronal induction...
November 2016: Genes to Cells: Devoted to Molecular & Cellular Mechanisms
https://www.readbyqxmd.com/read/27335169/ubiquitin-dependent-and-independent-roles-of-sumo-in-proteostasis
#15
Frauke Liebelt, Alfred C O Vertegaal
Cellular proteomes are continuously undergoing alterations as a result of new production of proteins, protein folding, and degradation of proteins. The proper equilibrium of these processes is known as proteostasis, implying that proteomes are in homeostasis. Stress conditions can affect proteostasis due to the accumulation of misfolded proteins as a result of overloading the degradation machinery. Proteostasis is affected in neurodegenerative diseases like Alzheimer's disease, Parkinson's disease, and multiple polyglutamine disorders including Huntington's disease...
August 1, 2016: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/27182943/long-term-memory-in-drosophila-is-influenced-by-histone-deacetylase-hdac4-interacting-with-sumo-conjugating-enzyme-ubc9
#16
Silvia Schwartz, Mauro Truglio, Maxwell J Scott, Helen L Fitzsimons
HDAC4 is a potent memory repressor with overexpression of wild type or a nuclear-restricted mutant resulting in memory deficits. Interestingly, reduction of HDAC4 also impairs memory via an as yet unknown mechanism. Although histone deacetylase family members are important mediators of epigenetic mechanisms in neurons, HDAC4 is predominantly cytoplasmic in the brain and there is increasing evidence for interactions with nonhistone proteins, suggesting HDAC4 has roles beyond transcriptional regulation. To that end, we performed a genetic interaction screen in Drosophila and identified 26 genes that interacted with HDAC4, including Ubc9, the sole SUMO E2-conjugating enzyme...
July 2016: Genetics
https://www.readbyqxmd.com/read/27177020/the-activity-of-the-glucocorticoid-receptor-is-regulated-by-sumo-conjugation-to-fkbp51
#17
M Antunica-Noguerol, M L Budziñski, J Druker, N C Gassen, M C Sokn, S Senin, F Aprile-Garcia, F Holsboer, T Rein, A C Liberman, E Arzt
FK506-binding protein 51 (FKBP51) regulates the activity of the glucocorticoid receptor (GR), and is therefore a key mediator of the biological actions of glucocorticoids. However, the understanding of the molecular mechanisms that govern its activity remains limited. Here, we uncover a novel regulatory switch for GR activity by the post-translational modification of FKBP51 with small ubiquitin-like modifier (SUMO). The major SUMO-attachment site, lysine 422, is required for FKBP51-mediated inhibition of GR activity in hippocampal neuronal cells...
October 2016: Cell Death and Differentiation
https://www.readbyqxmd.com/read/27146268/pias1-regulates-mutant-huntingtin-accumulation-and-huntington-s-disease-associated-phenotypes-in%C3%A2-vivo
#18
Joseph Ochaba, Alex Mas Monteys, Jacqueline G O'Rourke, Jack C Reidling, Joan S Steffan, Beverly L Davidson, Leslie M Thompson
The disruption of protein quality control networks is central to pathology in Huntington's disease (HD) and other neurodegenerative disorders. The aberrant accumulation of insoluble high-molecular-weight protein complexes containing the Huntingtin (HTT) protein and SUMOylated protein corresponds to disease manifestation. We previously identified an HTT-selective E3 SUMO ligase, PIAS1, that regulates HTT accumulation and SUMO modification in cells. Here we investigated whether PIAS1 modulation in neurons alters HD-associated phenotypes in vivo...
May 4, 2016: Neuron
https://www.readbyqxmd.com/read/27087120/global-sumoylation-facilitates-the-multimodal-neuroprotection-afforded-by-quercetin-against-the-deleterious-effects-of-oxygen-glucose-deprivation-and-the-restoration-of-oxygen-glucose
#19
Yang-Ja Lee, Joshua D Bernstock, Nandakumar Nagaraja, Brian Ko, John M Hallenbeck
The putative neuroprotective properties of various flavonoids have long been reported. Among this class of chemicals, quercetin, a major flavone/flavonol naturally occurring in plants, deserves focused attention because of the myriad of beneficial effects observed in various in vitro and in vivo models of central nervous system damage/degeneration. However, the mechanisms governing the beneficial outcomes mediated by quercetin remain to be elucidated. In an effort to define the underlying molecular mechanisms, our study employed human/rat neuroblastoma cell lines (SHSY5Y and B35, respectively) and E18-derived rat primary cortical neurons upon which the effects of various flavonoids were examined...
July 2016: Journal of Neurochemistry
https://www.readbyqxmd.com/read/27039038/the-sumo-protease-senp7-is-required-for-proper-neuronal-differentiation
#20
Francisco Juarez-Vicente, Noelia Luna-Pelaez, Mario Garcia-Dominguez
Covalent attachment of the Small ubiquitin-like modifier (Sumo) polypeptide to proteins regulates many processes in the eukaryotic cell. In the nervous system, Sumo has been associated with the synapsis and with neurodegenerative diseases. However, its involvement in regulating neuronal differentiation remains largely unknown. Here we show that net Sumo deconjugation is observed during neurogenesis and that Sumo overexpression impairs this process. In an attempt to shed light on the underlying mechanisms, we have analyzed the expression profile of genes coding for components of the sumoylation pathway following induction of neuronal differentiation...
July 2016: Biochimica et Biophysica Acta
keyword
keyword
25121
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"