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  1. Article ; Online: CPEB3-dependent increase in GluA2 subunits impairs excitatory transmission onto inhibitory interneurons in a mouse model of fragile X.

    Hwang, Jee-Yeon / Monday, Hannah R / Yan, Jingqi / Gompers, Andrea / Buxbaum, Adina R / Sawicka, Kirsty J / Singer, Robert H / Castillo, Pablo E / Zukin, R Suzanne

    Cell reports

    2022  Volume 39, Issue 10, Page(s) 110853

    Abstract: Fragile X syndrome (FXS) is a leading cause of inherited intellectual disability and autism. Whereas dysregulated RNA translation in Fmr1 knockout (KO) mice, a model of FXS, is well studied, little is known about aberrant transcription. Using single- ... ...

    Abstract Fragile X syndrome (FXS) is a leading cause of inherited intellectual disability and autism. Whereas dysregulated RNA translation in Fmr1 knockout (KO) mice, a model of FXS, is well studied, little is known about aberrant transcription. Using single-molecule mRNA detection, we show that mRNA encoding the AMPAR subunit GluA2 (but not GluA1) is elevated in dendrites and at transcription sites of hippocampal neurons of Fmr1 KO mice, indicating elevated GluA2 transcription. We identify CPEB3, a protein implicated in memory consolidation, as an upstream effector critical to GluA2 mRNA expression in FXS. Increased GluA2 mRNA is translated into an increase in GluA2 subunits, a switch in synaptic AMPAR phenotype from GluA2-lacking, Ca
    MeSH term(s) Animals ; Disease Models, Animal ; Fragile X Mental Retardation Protein/metabolism ; Fragile X Syndrome/genetics ; Interneurons/metabolism ; Mice ; Mice, Knockout ; RNA, Messenger/metabolism ; RNA-Binding Proteins/genetics ; Receptors, AMPA/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/metabolism
    Chemical Substances Cpeb3 protein, mouse ; Fmr1 protein, mouse ; RNA, Messenger ; RNA-Binding Proteins ; Receptors, AMPA ; Receptors, N-Methyl-D-Aspartate ; Fragile X Mental Retardation Protein (139135-51-6)
    Language English
    Publishing date 2022-06-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2022.110853
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Neuroinflammatory transcriptional programs induced in rhesus pre-frontal cortex white matter during acute SHIV infection.

    Hawes, Chase E / Elizaldi, Sonny R / Beckman, Danielle / Diniz, Giovanne B / Shaan Lakshmanappa, Yashavanth / Ott, Sean / Durbin-Johnson, Blythe P / Dinasarapu, Ashok R / Gompers, Andrea / Morrison, John H / Iyer, Smita S

    Journal of neuroinflammation

    2022  Volume 19, Issue 1, Page(s) 250

    Abstract: Background: Immunosurveillance of the central nervous system (CNS) is vital to resolve infection and injury. However, immune activation within the CNS in the setting of chronic viral infections, such as HIV-1, is strongly linked to progressive ... ...

    Abstract Background: Immunosurveillance of the central nervous system (CNS) is vital to resolve infection and injury. However, immune activation within the CNS in the setting of chronic viral infections, such as HIV-1, is strongly linked to progressive neurodegeneration and cognitive decline. Establishment of HIV-1 in the CNS early following infection underscores the need to delineate features of acute CNS immune activation, as these early inflammatory events may mediate neurodegenerative processes. Here, we focused on elucidating molecular programs of neuroinflammation in brain regions based on vulnerability to neuroAIDS and/or neurocognitive decline. To this end, we assessed transcriptional profiles within the subcortical white matter of the pre-frontal cortex (PFCw), as well as synapse dense regions from hippocampus, superior temporal cortex, and caudate nucleus, in rhesus macaques following infection with Simian/Human Immunodeficiency Virus (SHIV.C.CH505).
    Methods: We performed RNA extraction and sequenced RNA isolated from 3 mm brain punches. Viral RNA was quantified in the brain and cerebrospinal fluid by RT-qPCR assays targeting SIV Gag. Neuroinflammation was assessed by flow cytometry and multiplex ELISA assays.
    Results: RNA sequencing and flow cytometry data demonstrated immune surveillance of the rhesus CNS by innate and adaptive immune cells during homeostasis. Following SHIV infection, viral entry and integration within multiple brain regions demonstrated vulnerabilities of key cognitive and motor function brain regions to HIV-1 during the acute phase of infection. SHIV-induced transcriptional alterations were concentrated to the PFCw and STS with upregulation of gene expression pathways controlling innate and T-cell inflammatory responses. Within the PFCw, gene modules regulating microglial activation and T cell differentiation were induced at 28 days post-SHIV infection, with evidence for stimulation of immune effector programs characteristic of neuroinflammation. Furthermore, enrichment of pathways regulating mitochondrial respiratory capacity, synapse assembly, and oxidative and endoplasmic reticulum stress were observed. These acute neuroinflammatory features were substantiated by increased influx of activated T cells into the CNS.
    Conclusions: Our data show pervasive immune surveillance of the rhesus CNS at homeostasis and reveal perturbations of important immune, neuronal, and synaptic pathways within key anatomic regions controlling cognition and motor function during acute HIV infection. These findings provide a valuable framework to understand early molecular features of HIV associated neurodegeneration.
    MeSH term(s) Animals ; Frontal Lobe ; HIV Infections ; HIV-1/genetics ; Humans ; Macaca mulatta/genetics ; RNA, Viral ; Simian Acquired Immunodeficiency Syndrome ; Simian Immunodeficiency Virus ; Viral Load ; White Matter
    Chemical Substances RNA, Viral
    Language English
    Publishing date 2022-10-06
    Publishing country England
    Document type Journal Article
    ZDB-ID 2156455-3
    ISSN 1742-2094 ; 1742-2094
    ISSN (online) 1742-2094
    ISSN 1742-2094
    DOI 10.1186/s12974-022-02610-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Deletion of a non-canonical regulatory sequence causes loss of Scn1a expression and epileptic phenotypes in mice.

    Haigh, Jessica L / Adhikari, Anna / Copping, Nycole A / Stradleigh, Tyler / Wade, A Ayanna / Catta-Preta, Rinaldo / Su-Feher, Linda / Zdilar, Iva / Morse, Sarah / Fenton, Timothy A / Nguyen, Anh / Quintero, Diana / Agezew, Samrawit / Sramek, Michael / Kreun, Ellie J / Carter, Jasmine / Gompers, Andrea / Lambert, Jason T / Canales, Cesar P /
    Pennacchio, Len A / Visel, Axel / Dickel, Diane E / Silverman, Jill L / Nord, Alex S

    Genome medicine

    2021  Volume 13, Issue 1, Page(s) 69

    Abstract: Background: Genes with multiple co-active promoters appear common in brain, yet little is known about functional requirements for these potentially redundant genomic regulatory elements. SCN1A, which encodes the Na: Methods: To determine the ... ...

    Abstract Background: Genes with multiple co-active promoters appear common in brain, yet little is known about functional requirements for these potentially redundant genomic regulatory elements. SCN1A, which encodes the Na
    Methods: To determine the functional role of one of these potentially redundant Scn1a promoters, we focused on the non-coding Scn1a 1b regulatory region, previously described as a non-canonical alternative transcriptional start site. We generated a transgenic mouse line with deletion of the extended evolutionarily conserved 1b non-coding interval and characterized changes in gene and protein expression, and assessed seizure activity and alterations in behavior.
    Results: Mice harboring a deletion of the 1b non-coding interval exhibited surprisingly severe reductions of Scn1a and Na
    Conclusions: This work contributes to functional dissection of the regulatory wiring of a major epilepsy risk gene, SCN1A. We identified the 1b region as a critical disease-relevant regulatory element and provide evidence that non-canonical and seemingly redundant promoters can have essential function.
    MeSH term(s) Animals ; Attention ; Base Sequence ; Brain/metabolism ; Brain/pathology ; Chromatin/metabolism ; Conserved Sequence/genetics ; Disease Models, Animal ; Electroencephalography ; Epilepsy/diagnostic imaging ; Epilepsy/genetics ; Evolution, Molecular ; Female ; Gene Expression Regulation ; HEK293 Cells ; Heterozygote ; Homozygote ; Humans ; Male ; Maze Learning ; Memory Disorders/genetics ; Mice, Inbred C57BL ; NAV1.1 Voltage-Gated Sodium Channel/genetics ; Neurons/metabolism ; Open Field Test ; Phenotype ; Protein Binding ; Regulatory Sequences, Nucleic Acid/genetics ; Sequence Deletion/genetics ; Survival Analysis ; Temperature ; Trans-Activators/metabolism ; Mice
    Chemical Substances Chromatin ; NAV1.1 Voltage-Gated Sodium Channel ; Scn1a protein, mouse ; Trans-Activators
    Language English
    Publishing date 2021-04-26
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2484394-5
    ISSN 1756-994X ; 1756-994X
    ISSN (online) 1756-994X
    ISSN 1756-994X
    DOI 10.1186/s13073-021-00884-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Germline Chd8 haploinsufficiency alters brain development in mouse.

    Gompers, Andrea L / Su-Feher, Linda / Ellegood, Jacob / Copping, Nycole A / Riyadh, M Asrafuzzaman / Stradleigh, Tyler W / Pride, Michael C / Schaffler, Melanie D / Wade, A Ayanna / Catta-Preta, Rinaldo / Zdilar, Iva / Louis, Shreya / Kaushik, Gaurav / Mannion, Brandon J / Plajzer-Frick, Ingrid / Afzal, Veena / Visel, Axel / Pennacchio, Len A / Dickel, Diane E /
    Lerch, Jason P / Crawley, Jacqueline N / Zarbalis, Konstantinos S / Silverman, Jill L / Nord, Alex S

    Nature neuroscience

    2017  Volume 20, Issue 8, Page(s) 1062–1073

    Abstract: The chromatin remodeling gene CHD8 represents a central node in neurodevelopmental gene networks implicated in autism. We examined the impact of germline heterozygous frameshift Chd8 mutation on neurodevelopment in mice. ... ...

    Abstract The chromatin remodeling gene CHD8 represents a central node in neurodevelopmental gene networks implicated in autism. We examined the impact of germline heterozygous frameshift Chd8 mutation on neurodevelopment in mice. Chd8
    MeSH term(s) Animals ; Brain/metabolism ; Cell Cycle Proteins/genetics ; Chromatin/metabolism ; DNA-Binding Proteins/genetics ; Gene Expression Regulation, Developmental/genetics ; Gene Regulatory Networks/genetics ; Haploinsufficiency/genetics ; Mice, Transgenic ; Mutation/genetics ; Phenotype ; Transcription Factors/genetics
    Chemical Substances Cell Cycle Proteins ; Chromatin ; DNA-Binding Proteins ; Transcription Factors ; duplin protein, mouse
    Language English
    Publishing date 2017-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1420596-8
    ISSN 1546-1726 ; 1097-6256
    ISSN (online) 1546-1726
    ISSN 1097-6256
    DOI 10.1038/nn.4592
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4891: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 67: Show issues

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  5. Article ; Online: miR-302b maintains "stemness" of human embryonal carcinoma cells by post-transcriptional regulation of Cyclin D2 expression.

    Lee, Nan Sook / Kim, Jong Soo / Cho, Wha Ja / Lee, Man Ryul / Steiner, Riley / Gompers, Andrea / Ling, Daijun / Zhang, Jae / Strom, Pl / Behlke, Mark / Moon, Sung-Hwan / Salvaterra, Paul M / Jove, Richard / Kim, Kye-Seong

    Biochemical and biophysical research communications

    2008  Volume 377, Issue 2, Page(s) 434–440

    Abstract: Embryonic stem cells (ESCs) and embryonal carcinoma cells (ECCs) possess the remarkable property of self-renewal and differentiation potency. They are model preparations for investigating the underlying mechanisms of "stemness". microRNAs are recently ... ...

    Abstract Embryonic stem cells (ESCs) and embryonal carcinoma cells (ECCs) possess the remarkable property of self-renewal and differentiation potency. They are model preparations for investigating the underlying mechanisms of "stemness". microRNAs are recently discovered small noncoding RNAs with a broad spectrum of functions, especially in control of development. Here, we show that miR-302b indirectly regulates expression of the pluripotent stem cell marker Oct4, and it directly regulates expression of Cyclin D2 protein, a developmental regulator during gastrulation. Using loss-of function and gain-of function approaches, we demonstrate that functional miR-302b is necessary to maintain stem cell self-renewal and inhibit neuronal differentiation of human ECCs. During retinoic acid-induced neuronal differentiation, Cyclin D2 protein but not mRNA expression is strongly increased, concurrent with the down-regulation of miR-302b and Oct4. Our results suggest that miR-302b plays an important role in maintaining the pluripotency of ECCs and probably ESCs, by post-transcriptional regulation of Cyclin D2 expression.
    MeSH term(s) Cell Differentiation ; Cell Line, Tumor ; Cyclin D2 ; Cyclins/biosynthesis ; Cyclins/genetics ; Embryonal Carcinoma Stem Cells/cytology ; Embryonal Carcinoma Stem Cells/metabolism ; Gene Expression Regulation ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; MicroRNAs/physiology ; Pluripotent Stem Cells/cytology ; Pluripotent Stem Cells/metabolism ; Protein Biosynthesis/genetics ; RNA, Messenger/biosynthesis ; Transcriptional Activation
    Chemical Substances CCND2 protein, human ; Cyclin D2 ; Cyclins ; MIRN302A microRNA, human ; MicroRNAs ; RNA, Messenger
    Language English
    Publishing date 2008-10-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2008.09.159
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 116: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
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