<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>288(23)</volume><submitter>Kugler JE</submitter><pubmed_abstract>The nuclei of most vertebrate cells contain members of the high mobility group N (HMGN) protein family, which bind specifically to nucleosome core particles and affect chromatin structure and function, including transcription. Here, we study the biological role of this protein family by systematic analysis of phenotypes and tissue transcription profiles in mice lacking functional HMGN variants. Phenotypic analysis of Hmgn1(tm1/tm1), Hmgn3(tm1/tm1), and Hmgn5(tm1/tm1) mice and their wild type littermates with a battery of standardized tests uncovered variant-specific abnormalities. Gene expression analysis of four different tissues in each of the Hmgn(tm1/tm1) lines reveals very little overlap between genes affected by specific variants in different tissues. Pathway analysis reveals that lo</pubmed_abstract><journal>The Journal of biological chemistry</journal><pagination>16690-16703</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3675603</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>High mobility group N proteins modulate the fidelity of the cellular transcriptional profile in a tissue- and variant-specific manner.</pubmed_title><pmcid>PMC3675603</pmcid><pubmed_authors>Bohla A</pubmed_authors><pubmed_authors>Becker L</pubmed_authors><pubmed_authors>Huang D</pubmed_authors><pubmed_authors>Horsch M</pubmed_authors><pubmed_authors>Ollert M</pubmed_authors><pubmed_authors>Gailus-Durner V</pubmed_authors><pubmed_authors>Adler T</pubmed_authors><pubmed_authors>Wolf E</pubmed_authors><pubmed_authors>Rathkolb B</pubmed_authors><pubmed_authors>Prehn C</pubmed_authors><pubmed_authors>Furusawa T</pubmed_authors><pubmed_authors>Kugler JE</pubmed_authors><pubmed_authors>Busch DH</pubmed_authors><pubmed_authors>Racz I</pubmed_authors><pubmed_authors>Eickelberg O</pubmed_authors><pubmed_authors>Yildirim AO</pubmed_authors><pubmed_authors>Hrabe de Angelis M</pubmed_authors><pubmed_authors>Stoger T</pubmed_authors><pubmed_authors>Aguilar-Pimentel JA</pubmed_authors><pubmed_authors>Holter SM</pubmed_authors><pubmed_authors>Garfinkel B</pubmed_authors><pubmed_authors>Wurst W</pubmed_authors><pubmed_authors>Ovcharenko I</pubmed_authors><pubmed_authors>Bustin M</pubmed_authors><pubmed_authors>Orly J</pubmed_authors><pubmed_authors>Adamski J</pubmed_authors><pubmed_authors>Garrett L</pubmed_authors><pubmed_authors>Fuchs H</pubmed_authors><pubmed_authors>Rochman M</pubmed_authors><pubmed_authors>Beckers J</pubmed_authors><pubmed_authors>Zimmer A</pubmed_authors><pubmed_authors>Klopstock T</pubmed_authors></additional><is_claimable>false</is_claimable><name>High mobility group N proteins modulate the fidelity of the cellular transcriptional profile in a tissue- and variant-specific manner.</name><description>The nuclei of most vertebrate cells contain members of the high mobility group N (HMGN) protein family, which bind specifically to nucleosome core particles and affect chromatin structure and function, including transcription. Here, we study the biological role of this protein family by systematic analysis of phenotypes and tissue transcription profiles in mice lacking functional HMGN variants. Phenotypic analysis of Hmgn1(tm1/tm1), Hmgn3(tm1/tm1), and Hmgn5(tm1/tm1) mice and their wild type littermates with a battery of standardized tests uncovered variant-specific abnormalities. Gene expression analysis of four different tissues in each of the Hmgn(tm1/tm1) lines reveals very little overlap between genes affected by specific variants in different tissues. Pathway analysis reveals that lo</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Jun</publication><modification>2025-04-05T00:36:08.696Z</modification><creation>2019-06-05T18:43:25Z</creation></dates><accession>S-EPMC3675603</accession><cross_references><pubmed>23620591</pubmed><doi>10.1074/jbc.m113.463315</doi><doi>10.1074/jbc.M113.463315</doi></cross_references></HashMap>