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Journal of Molecular Cell Biology 2018年第6期10卷 515-526页

作者： Wei Zhang Guihai Feng Libin Wang Fei Teng Liu Wang Wei Li Ying Zhang Qi Zhou State Key Laboratory of Stem Cell and Reproductive Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China University of Chinese Academy of Sciences Beijing 100049China

The generation of induced pturipotent stem cells (iPSCs)offers a great opportunity in research and regenerative *** current poor efficiency and incomplete mechanistic understanding of the reprogramming process hamper the clinical application of iPSCs. mecp2 connects histone modification and DNA methyiation,which are key changes of somatic cell ***,the rote of mecp2 in celt reprogramming has not been *** this study,we found that mecp2 deficiency enhanced reprogramming efficiency and stimulated cell proliferation through regulating cell cycle protein expression in the earLy stage of ***2 deficiency enhanced the expression of ribosomal protein genes,thereby enhancing reprogramming efficiency through promoting the translation of ceLl cycle *** the end,mecp2 deficiency stimulated IGF1/AKT/mTOR signaling and activated ribosomal protein gene *** together,our data indicate that mecp2 deficiency promoted cell reprogramming through stimulating IGF1/AKT/mTOR signaling and activating ribosomal protein-mediated cell cycle gene translation in the early stage of reprogramming.

关键词： mecp2 cell reprogramming IGFI/AKT/mTOR signaling ribosomal protein cell cycle

Loss of O-GlcNAcylation on mecp2 at Threonine 203 Leads to Neurodevelopmental Disorders

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Neuroscience Bulletin 2022年第2期38卷 113-134页

作者： Juanxian Cheng Zhe Zhao Liping Chen Ying Li Ruijing Du Yan Wu Qian Zhu Ming Fan Xiaotao Duan Haitao Wu Department of Neurobiology Beijing Institute of Basic Medical SciencesBeijing 100850China Chinese Institute for Brain Research Beijing 102206China Key Laboratory of Neuroregeneration Co-innovation Center of NeuroregenerationNantong UniversityNantong 226019China State Key Laboratory of Toxicology and Medical Countermeasures Beijing Institute of Pharmacology and ToxicologyBeijing 100850China

Mutations of the X-linked methyl-CpG-binding protein 2(mecp2)gene in humans are responsible for most cases of Rett syndrome(RTT),an X-linked progressive neurological *** genome-wide screens in clinical trials have revealed several putative RTT-associ-ated mutations in mecp2,their causal relevance regarding the functional regulation of mecp2 at the etiologic sites at the protein level requires more *** this study,we demonstrated that mecp2 was dynamically modified by O-linked-P-N-acetylglucosamine(O-GlcNAc)at threonine 203(T203),an etiologic site in RTT *** of the O-GlcNAcylation of mecp2 specifically at T203 impaired dendrite development and spine maturation in cultured hippocampal neurons,and disrupted neuronal migration,dendritic spine morphogenesis,and caused dysfunction of synaptic transmission in the developing and juvenile mouse cerebral ***,genetic disruption of O-GlcNAcylation at T203 on mecp2 decreased the neuronal activity-induced induction of Bdnf *** study highlights the critical role of mecp2 T203 O-GlcNAcylation in neural development and synaptic transmission potentially via brain-derived neurotrophic factor.

关键词： mecp2 O-GlcNAcylation-Dendrite development Synaptic transmission Braiderived neurotrophic factor

Melatonin modifies SOX2^+ cell proliferation in dentate gyrus and modulates SIRT1 and mecp2 in long-term sleep deprivation

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Neural Regeneration Research 2019年第10期14卷 1787-1795页

作者： Alan Hinojosa-Godínez Luis F. Jave-Suarez Mario Flores-Soto Alma Y. Gálvez-Contreras Sonia Luquín Edith Oregon-Romero Oscar González-Pérez Rocio E. González-Castaneda Laboratorio de Microscopía de Alta Resolución Departamento de NeurocienciasCentro Universitario de Ciencias de la SaludUniversidad de GuadalajaraGuadalajaraMéxico Laboratorio de Neurociencias Facultad de PsicologíaUniversidad de ColimaColimaMéxico División de Inmunología Centro de Investigación Biomédica de OccidenteInstituto Mexicano del Seguro SocialGuadalajaraMéxico División de Neurociencias Centro de Investigación Biomédica de OccidenteInstituto Mexicano del Seguro SocialGuadalajaraMéxico Instituto de Investigación en Ciencias Biomédicas (IICB) Departamento de Biología Molecular y GenómicaCentro Universitario de Ciencias de la SaludUniversidad de GuadalajaraGuadalajaraMéxico Unidad de Atención en Neurociencias Departamento de Neurociencias. Centro Universitario de Ciencias de la SaludUniversidad de GuadalajaraGuadalajaraMéxico

Melatonin is a pleiotropic molecule that,after a short-term sleep deprivation,promotes the proliferation of neural stem cells in the adult ***,this effect has not been observed in long-term sleep *** precise mechanism exerted by melatonin on the modulation of neural stem cells is not entirely elucidated,but evidence indicates that epigenetic regulators may be involved in this *** this study,we investigated the effect of melatonin treatment during a 96-hour sleep deprivation and analyzed the expression of epigenetic modulators predicted by computational text mining and keyword *** results showed that the administration of melatonin under sleep-deprived conditions increased the mecp2 expression and reduced the SIRT1 expression in the dentate *** observed that let-7 b,mir-132,and mir-124 were highly expressed in the dentate gyrus after melatonin administration,but they were not modified by sleep *** addition,we found more Sox2^+/5-bromo-2’-deoxyuridine(BrdU)^+cells in the subgranular zone of the sleep-deprived group treated with melatonin than in the untreated *** findings may support the notion that melatonin modifies the expression of epigenetic mediators that,in turn,regulate the proliferation of neural progenitor cells in the adult dentate gyrus under long-term sleep-deprived *** procedures performed in this study were approved by the Animal Ethics Committee of the University of Guadalajara,Mexico(approval ***-16610)on January 2,2016.

关键词： sleep-deprivation melatonin microRNA neurogenesis Sirtuin 1 SIRT1 methyl-CpG-binding protein 2 mecp2 epigenetic text-mining mir-9 let-7b

Graded and pan-neural disease phenotypes of Rett Syndrome linked with dosage of functional mecp2

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Protein & Cell 2021年第8期12卷 639-652页

作者： Xiaoying Chen Xu Han Bruno Bianchi Wuqiang Guan Weihong Ge Yong-Chun Yu Yi E.Sun Shanghai Institute of Stem Cell Research and Clinical Translation Shanghai East HospitalTongji University School of MedicineShanghai 200120China State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science Institutes of Brain ScienceJing’an District Centre Hospital of ShanghaiFudan UniversityShanghai 200032China Department of Psychiatry and Biobehavioral Sciences David Geffen School of MedicineUCLALos AngelesCA 90095USA

Rett syndrome(RTT)is a progressive neurodevelop-mental disorder,mainly caused by mutations in mecp2 and currently with no *** report here that neurons from R106W mecp2 RTT human iPSCs as well as human embryonic stem cells after mecp2 knockdown exhibit consistent and long-lasting impairment in maturation as indicated by impaired action potentials and passive membrane properties as well as reduced soma size and spine ***,RTT-inherent defects in neuronal maturation could be pan-neuronal and occurred in neurons with both dorsal and ventral forebrain *** of mecp2 led to more severe neuronal deficits as compared to RTT iPSC-derived neurons,which appeared to retain partial ***,consistent deficits in nuclear size,dendritic complexity and circuitry-dependent spontaneous postsynaptic currents could only be observed in mecp2 knockdown neurons but not RTT iPSC-derived *** neuron-intrinsic and circuitry-dependent deficits of mecp2-deficient neurons could be fully or partially rescued by re-expression of wild type or T158M mecp2,strengthening the dosage dependency of mecp2 on disease phenotypes and also the partial function of the *** findings thus reveal stable neuronal maturation deficits and unexpectedly,graded sensitivities of neuron-inherent and neural transmission phenotypes towards the extent of mecp2 deficiency,which is informative for future therapeutic development.

关键词： mecp2 Rett Syndrome human pluripotent stem cell neural differentiation

MiR-130a regulates and dendritic spine mecp2 neurite outgrowth density by targeting

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Protein & Cell 2016年第7期7卷 489-500页

作者： Yunjia Zhang Mengmeng Chen Zilong Qiu Keping Hu Warren McGee Xiaoping Chen Jianghong Liu Li Zhu Jane Y. Wu State Key Laboratory for Brain & Cognitive Science Institute of Biophysics Chinese Academy of Sciences Beijing 100101 China University of Chinese Academy of Sciences Beijing 100049 China Laboratory of Molecular Basis of Neural Plasticity Institute of Neuroscience Chinese Academy of Sciences Shanghai 200031 China Institute of Medicinal Plant Development (IMPLAD) Chinese Academy of Medical Sciences Beijing 100193 China Department of Neurology Center for Genetic Medicine Lurie Cancer Center Northwestern University Feinberg School of Medicine Chicago IL 60611 USA

MicroRNAs （miRNAs） are critical for both development and function of the central nervous system. Significant evidence suggests that abnormal expression of miRNAs is associated with neurodevelopmental disorders. mecp2 protein is an epigenetic regulator repressing or activating gene transcription by binding to methylated DNA. Both loss-of-function and gain-of-function muta- tions in the mecp2 gene lead to neurodevelopmental disorders such as Rett syndrome, autism and mecp2 duplication syndrome. In this study, we demonstrate that miR-130a inhibits neurite outgrowth and reduces dendritic spine density as well as dendritic complexity. Bioinformatics analyses, cell cultures and biochemical experiments indicate that miR-130a targets mecp2 and down-regulates mecp2 protein expression. Further- more, expression of the wild-type mecp2, but not a loss- of-function mutant, rescues the miR-130a-induced phe- notype. Our study uncovers the mecp2 gene as a pre- vious unknown target for miR-130a, supporting that miR-130a may play a role in neurodevelopment by reg- ulating mecp2. Together with data from other groups,our work suggests that a feedback regulatory mecha- nism involving both miR-130a and mecp2 may serve to ensure their appropriate expression and function in neural development.

关键词： miR-130a mecp2 neurite outgrowth,dendritic spines dendrite morphology

Extension of the Lifespan of a Mouse Model of Rett Syndrome by Intracerebroventricular Delivery of mecp2

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Neuroscience Bulletin 2023年第2期39卷 297-302页

作者： Kan Yang Cheng Cheng Yiting Yuan Yuefang Zhang Shifang Shan Zilong Qiu Center for Excellence in Brain Science and Intelligence Technology Institute of NeuroscienceState Key Laboratory of NeuroscienceCAS Key Laboratory of Primate NeurobiologyChinese Academy of SciencesShanghai 200031China Belief BioMed(Shanghai) Co.Ltd.Shanghai 200032China National Clinical Research Center for Aging and Medicine Huashan HospitalFudan UniversityShanghai 200040China

DearEditors,Rett Syndrome(RTT)is a severe neurodevelopmental disorder characterized by neural dysfunctions and a reduced lifespan,mainly in female patients,involving loss-of-function mutations in the methyl-CpG bindin... 详细信息

关键词： mecp2 Extension neural

Regulation and function of stimulus-induced phosphorylation of mecp2

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Frontiers in Biology 2014年第5期9卷 367-375页

作者： Hongda LI Waisman Center University of Wisconsin-Madison Madison WI 53705 USA Genetics Training Program University of Wisconsin-Madison Madison WI 53 705 USA Department of Neurology University of Wisconsin-Madison Madison WI 53705 USA

DNA methylation-dependent epigenetic regulation plays important roles in the development and function of the mammalian nervous system. mecp2 is a key player in recognizing methylated DNA and interpreting the epigenetic information encoded in different DNA methylation patterns. Mutations in the mecp2 gene cause Rett syndrome, a devastating neurological disease that shares many features with autism. One interesting aspect of mecp2 function is that it can be phosphorylated in response to diverse stimuli. Insights into the regulation and function of mecp2 phosphorylation will help improve our understanding of how mecp2 integrates environmental stimuli in neuronal nuclei to generate adaptive responses and may eventually lead to treatments for patients.

关键词： mecp2 phosphorylation Rett syndrome

Gene Editing to the Rescue:Reversal of Social Deficits Associated with mecp2 Duplication

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Neuroscience Bulletin 2020年第6期36卷 567-569页

作者： Zi-Xian Yu Dan-Yang Wang Xiao-Hong Xu Institute of Neuroscience State Key Laboratory of NeuroscienceChinese Academy of Sciences Center for Excellence in Brain Science and Intelligence TechnologyChinese Academy of SciencesShanghai 200031China University of the Chinese Academy of Sciences Beijing 100049China Shanghai Center for Brain Science and Brain-Inspired Intelligence Technology Shanghai 200031China

Methyl-CpG-binding protein 2 (mecp2) is broadly recognized as the genetic cause of Rett Syndrome (RTT),a devastating neurodevelopmental disorder with the progressive loss in motor skills and speech that is found almost exclusively in young girls [1,2].Over 95%of RTT patients carry loss-of-function mutations in the X-linked mecp2gene,while the same mutations in males largely lead to infantile death.

关键词： mecp2 mecp2 Rescue

Overexpression of mecp2 in the Suprachiasmatic Nucleus Alters Circadian Rhythm and Induces Abnormal Social Behaviors

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Neuroscience Bulletin 2021年第12期37卷 1713-1717页

作者： Hailin Liu Zilong Qiu Center for Excellence in Brain Science and Intelligence Technology Institute of NeuroscienceState Key Laboratory of NeuroscienceCAS Key Laboratory of Primate NeurobiologyChinese Academy of SciencesShanghai 200031China University of Chinese Academy of Sciences Beijing 100049China Shanghai Center for Brain Science and Brain-Inspired Intelligence Technology Shanghai 201210China National Clinical Research Center for Aging and Medicine Huashan HospitalFudan UniversityShanghai 200040China

Dear Editors,Autism spectrum disorder is a highly heritable neurodevel-opmental disorder and is often associated with sleep disorders and dysregulation of the circadian rhythm[1,2].Whether neural circuits governing the circadian rhythm are causally associated with social behaviors remains to be *** this work,we used mice with mecp2 duplication as a model of autism to investigate whether regulation of the circadian rhythm is connected to social behaviors.

关键词： mecp2 rhythm connected

Structural investigation of Rett-inducing mecp2 mutations

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Genes & Diseases 2019年第1期6卷 31-34页

作者： Ottavia Spiga Simone Gardini Nicole Rossi Vittoria Cicaloni Francesco Pettini Neri Niccolai Annalisa Santucci Department of Biotechnology Chemistry and PharmacyUniversity of SienaSiena53100Italy GenomeUp SRL Rome00199Italy Toscana Life Sciences Foundation(TLS) Siena 53100Italy

X-ray structure of methyl-CpG binding domain(MBD)of mecp2,an intrinsically disordered protein(IDP)involved in Rett syndrome,offers a rational basis for defining the spatial distribution for most of the sites where mutations responsible of Rett syndrome,RTT,*** have ascribed pathogenicity for mutations of amino acids bearing positively charged side chains,all located at the protein-DNA interface,as positive charge removal cause reduction of the mecp2-DNA adduct *** of the frequent proline replacements,outside the DNA contact moiety of MBD,can be attributed to the role of this amino acid for maintaining both unfolded states for unbound mecp2 and,at the same time,to favor some higher conformational order for stabilizing structural determinants required by protein *** hypotheses can be extended to transcription repressor domain,TRD,the other mecp2-DNA interaction site and,in general,to all the IDP that interact with nucleic acids.

关键词： DNA binding domains mecp2 Mutation distribution Protein structure Rett syndrome