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dc.contributor.authorJiang, Yan
dc.contributor.authorJakovcevski, Mira
dc.contributor.authorBharadwaj, Rahul
dc.contributor.authorConnor, Caroline M.
dc.contributor.authorSchroeder, Frederick Albert
dc.contributor.authorLin, Cong L.
dc.contributor.authorStraubhaar, Juerg R.
dc.contributor.authorMartin, Gilles E.
dc.contributor.authorAkbarian, Schahram
dc.date2022-08-11T08:08:54.000
dc.date.accessioned2022-08-23T16:11:23Z
dc.date.available2022-08-23T16:11:23Z
dc.date.issued2010-05-28
dc.date.submitted2011-05-20
dc.identifier.citation<p>J Neurosci. 2010 May 26;30(21):7152-67. <a href="http://dx.doi.org/10.1523/JNEUROSCI.1314-10.2010">Link to article on publisher's site</a></p>
dc.identifier.issn0270-6474 (Linking)
dc.identifier.doi10.1523/JNEUROSCI.1314-10.2010
dc.identifier.pmid20505083
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33153
dc.description.abstractHistone methyltransferases specific for the histone H3-lysine 9 residue, including Setdb1 (Set domain, bifurcated 1)/Eset/Kmt1e are associated with repressive chromatin remodeling and expressed in adult brain, but potential effects on neuronal function and behavior remain unexplored. Here, we report that transgenic mice with increased Setdb1 expression in adult forebrain neurons show antidepressant-like phenotypes in behavioral paradigms for anhedonia, despair, and learned helplessness. Chromatin immunoprecipitation in conjunction with DNA tiling arrays (ChIP-chip) revealed that genomic occupancies of neuronal Setdb1 are limited to
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=20505083&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsPublisher PDF posted after 6 months as allowed by the publisher's author rights policy at http://www.jneurosci.org/sites/default/files/files/JN_License_to_Publish.pdf.
dc.subjectAdaptation, Ocular; Affect; Age Factors; Animals; Animals, Newborn; Avoidance Learning; Behavior, Animal; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Cells, Cultured; Chromatin; Chromatin Immunoprecipitation; Conditioning (Psychology); Electroshock; Excitatory Amino Acid Agents; Excitatory Postsynaptic Potentials; Exploratory Behavior; Fear; Food Preferences; Gene Expression Regulation; Green Fluorescent Proteins; Hippocampus; Humans; Immobility Response, Tonic; Maze Learning; Membrane Potentials; Mice; Mice, Inbred C57BL; Mice, Transgenic; Motor Activity; Neurons; Patch-Clamp Techniques; Protein Methyltransferases; RNA, Small Interfering; Receptors, N-Methyl-D-Aspartate; Sucrose; Sweetening Agents; Transfection
dc.subjectNeuroscience and Neurobiology
dc.titleSetdb1 histone methyltransferase regulates mood-related behaviors and expression of the NMDA receptor subunit NR2B
dc.typeJournal Article
dc.source.journaltitleThe Journal of neuroscience : the official journal of the Society for Neuroscience
dc.source.volume30
dc.source.issue21
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2704&amp;context=gsbs_sp&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1694
dc.identifier.contextkey2022700
refterms.dateFOA2022-08-23T16:11:23Z
html.description.abstract<p>Histone methyltransferases specific for the histone H3-lysine 9 residue, including Setdb1 (Set domain, bifurcated 1)/Eset/Kmt1e are associated with repressive chromatin remodeling and expressed in adult brain, but potential effects on neuronal function and behavior remain unexplored. Here, we report that transgenic mice with increased Setdb1 expression in adult forebrain neurons show antidepressant-like phenotypes in behavioral paradigms for anhedonia, despair, and learned helplessness. Chromatin immunoprecipitation in conjunction with DNA tiling arrays (ChIP-chip) revealed that genomic occupancies of neuronal Setdb1 are limited to</p>
dc.identifier.submissionpathgsbs_sp/1694
dc.contributor.departmentMartin Lab
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentBrudnick Neuropsychiatric Research Institute
dc.contributor.departmentDepartment of Psychiatry
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages7152-67
dc.contributor.studentYan Jiang; Caroline Connor; Frederick Schroeder


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