<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Andresini O</submitter><funding>Sapienza Università di Roma</funding><pagination>8</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6334472</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>The cell-cycle inhibitor p57&lt;sup>kip2&lt;/sup> plays a critical role in mammalian development by coordinating cell proliferation and differentiation in many cell types. p57&lt;sup>kip2&lt;/sup> expression is finely regulated by several epigenetic mechanisms, including paternal imprinting. Kcnq1ot1, a long non-coding RNA (LncRNA), whose gene maps to the p57&lt;sup>Kip2&lt;/sup> imprinting domain, is expressed exclusively from the paternal allele and participates in the cis-silencing of the neighboring imprinted genes through chromatin-level regulation. In light of our previous evidence of a functional interaction between myogenic factors and imprinting control elements in the regulation of the maternal p57&lt;sup>Kip2&lt;/sup> allele during muscle differentiation, we examined the possibility </pubmed_abstract><journal>Epigenetics &amp; chromatin</journal><pubmed_title>The long non-coding RNA Kcnq1ot1 controls maternal p57 expression in muscle cells by promoting H3K27me3 accumulation to an intragenic MyoD-binding region.</pubmed_title><pmcid>PMC6334472</pmcid><funding_grant_id>RM11715C642DFF3B</funding_grant_id><funding_grant_id>RP116154C9BD387B</funding_grant_id><pubmed_authors>Maione R</pubmed_authors><pubmed_authors>Rossi MN</pubmed_authors><pubmed_authors>Andresini O</pubmed_authors><pubmed_authors>Petrai S</pubmed_authors><pubmed_authors>Santini T</pubmed_authors><pubmed_authors>Matteini F</pubmed_authors></additional><is_claimable>false</is_claimable><name>The long non-coding RNA Kcnq1ot1 controls maternal p57 expression in muscle cells by promoting H3K27me3 accumulation to an intragenic MyoD-binding region.</name><description>&lt;h4>Background&lt;/h4>The cell-cycle inhibitor p57&lt;sup>kip2&lt;/sup> plays a critical role in mammalian development by coordinating cell proliferation and differentiation in many cell types. p57&lt;sup>kip2&lt;/sup> expression is finely regulated by several epigenetic mechanisms, including paternal imprinting. Kcnq1ot1, a long non-coding RNA (LncRNA), whose gene maps to the p57&lt;sup>Kip2&lt;/sup> imprinting domain, is expressed exclusively from the paternal allele and participates in the cis-silencing of the neighboring imprinted genes through chromatin-level regulation. In light of our previous evidence of a functional interaction between myogenic factors and imprinting control elements in the regulation of the maternal p57&lt;sup>Kip2&lt;/sup> allele during muscle differentiation, we examined the possibility </description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Jan</publication><modification>2026-07-16T16:25:27.462Z</modification><creation>2025-05-18T11:32:13.403Z</creation></dates><accession>S-EPMC6334472</accession><cross_references><pubmed>30651140</pubmed><doi>10.1186/s13072-019-0253-1</doi></cross_references></HashMap>