{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Velasco-Aviles S"],"funding":["ISABIAL","Conselleria de Cultura, Educación y Ciencia, Generalitat Valenciana","Ministerio de Economía y Competitividad","Ministerio de Educación, Cultura y Deporte","Wellcome Trust"],"pagination":["e72917"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8853665"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11"],"pubmed_abstract":["The class IIa histone deacetylases (HDACs) have pivotal roles in the development of different tissues. Of this family, Schwann cells express <i>Hdac4</i>, <i>5</i>, and <i>7</i> but not <i>Hdac9</i>. Here, we show that a transcription factor regulated genetic compensatory mechanism within this family of proteins, blocks negative regulators of myelination ensuring peripheral nerve developmental myelination and remyelination after injury. Thus, when <i>Hdac4</i> and <i>5</i> are knocked-out from Schwann cells in mice, a JUN-dependent mechanism induces the compensatory overexpression of <i>Hdac7</i> permitting, although with a delay, the formation of the myelin sheath. When <i>Hdac4</i>, <i>5</i>, and <i>7</i> are simultaneously removed, the myocyte-specific enhancer-factor d (MEF2D) binds to"],"journal":["eLife"],"pubmed_title":["A genetic compensatory mechanism regulated by &lt;i&gt;Jun&lt;/i&gt; and &lt;i&gt;Mef2d&lt;/i&gt; modulates the expression of distinct class IIa &lt;i&gt;Hdacs&lt;/i&gt; to ensure peripheral nerve myelination and repair."],"pmcid":["PMC8853665"],"funding_grant_id":["206634/Z/17/Z","FPU16/00283","PID2019-109762RB-I00","UGP18-257","ACIF/2 017/169","BFU2016-75864R","PROMETEO 2018/114","UGP-2019-128"],"pubmed_authors":["Casillas-Bajo A","Cabedo H","Patel N","Frutos-Rincon L","Velasco-Aviles S","Gomez-Sanchez JA","Velasco E","Gallar J","Arthur-Farraj P"],"additional_accession":[]},"is_claimable":false,"name":"A genetic compensatory mechanism regulated by &lt;i&gt;Jun&lt;/i&gt; and &lt;i&gt;Mef2d&lt;/i&gt; modulates the expression of distinct class IIa &lt;i&gt;Hdacs&lt;/i&gt; to ensure peripheral nerve myelination and repair.","description":"The class IIa histone deacetylases (HDACs) have pivotal roles in the development of different tissues. Of this family, Schwann cells express <i>Hdac4</i>, <i>5</i>, and <i>7</i> but not <i>Hdac9</i>. Here, we show that a transcription factor regulated genetic compensatory mechanism within this family of proteins, blocks negative regulators of myelination ensuring peripheral nerve developmental myelination and remyelination after injury. Thus, when <i>Hdac4</i> and <i>5</i> are knocked-out from Schwann cells in mice, a JUN-dependent mechanism induces the compensatory overexpression of <i>Hdac7</i> permitting, although with a delay, the formation of the myelin sheath. When <i>Hdac4</i>, <i>5</i>, and <i>7</i> are simultaneously removed, the myocyte-specific enhancer-factor d (MEF2D) binds to","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jan","modification":"2026-05-30T23:15:49.822Z","creation":"2024-11-06T06:43:35.632Z"},"accession":"S-EPMC8853665","cross_references":{"pubmed":["35076395"],"doi":["10.7554/eLife.72917"]}}