<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ishikawa M</submitter><funding>Diabetes Australia Research Trust</funding><funding>National Health and Medical Research Council</funding><funding>Australian Research Council</funding><pagination>759-775</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7894545</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>73(2)</volume><pubmed_abstract>&lt;h4>Background and aims&lt;/h4>Growth hormone (GH) is important for liver regeneration after partial hepatectomy (PHx). We investigated this process in C57BL/6 mice that express different forms of the GH receptor (GHR) with deletions in key signaling domains.&lt;h4>Approach and results&lt;/h4>PHx was performed on C57BL/6 mice lacking GHR (Ghr&lt;sup>-/-&lt;/sup> ), disabled for all GH-dependent Janus kinase 2 signaling (Box1&lt;sup>-/-&lt;/sup> ), or lacking only GH-dependent signal transducer and activator of transcription 5 (STAT5) signaling (Ghr391&lt;sup>-/-&lt;/sup> ), and wild-type littermates. C57BL/6 Ghr&lt;sup>-/-&lt;/sup> mice showed striking mortality within 48 hours after PHx, whereas Box1&lt;sup>-/-&lt;/sup> or Ghr391&lt;sup>-/-&lt;/sup> mice survived with normal liver regeneration. Ghr&lt;sup>-/-&lt;/sup> mortality was associ</pubmed_abstract><journal>Hepatology (Baltimore, Md.)</journal><pubmed_title>Growth Hormone Stops Excessive Inflammation After Partial Hepatectomy, Allowing Liver Regeneration and Survival Through Induction of H2-Bl/HLA-G.</pubmed_title><pmcid>PMC7894545</pmcid><funding_grant_id>APP1025094</funding_grant_id><funding_grant_id>Centre of Excellence in Convergent Bio‐Nano Scienc</funding_grant_id><funding_grant_id>APP1156489</funding_grant_id><funding_grant_id>APP1025082</funding_grant_id><funding_grant_id>APP1124026</funding_grant_id><funding_grant_id>postdoctoral fellowship</funding_grant_id><pubmed_authors>Ishikawa M</pubmed_authors><pubmed_authors>Rossjohn J</pubmed_authors><pubmed_authors>Chhabra Y</pubmed_authors><pubmed_authors>Tunny KA</pubmed_authors><pubmed_authors>Ho KKY</pubmed_authors><pubmed_authors>Brooks AJ</pubmed_authors><pubmed_authors>Medina J</pubmed_authors><pubmed_authors>Fernandez-Rojo MA</pubmed_authors><pubmed_authors>Parton RG</pubmed_authors><pubmed_authors>Minami S</pubmed_authors><pubmed_authors>Chikani V</pubmed_authors><pubmed_authors>Waters MJ</pubmed_authors><pubmed_authors>Ramm GA</pubmed_authors><pubmed_authors>Vivian JP</pubmed_authors></additional><is_claimable>false</is_claimable><name>Growth Hormone Stops Excessive Inflammation After Partial Hepatectomy, Allowing Liver Regeneration and Survival Through Induction of H2-Bl/HLA-G.</name><description>&lt;h4>Background and aims&lt;/h4>Growth hormone (GH) is important for liver regeneration after partial hepatectomy (PHx). We investigated this process in C57BL/6 mice that express different forms of the GH receptor (GHR) with deletions in key signaling domains.&lt;h4>Approach and results&lt;/h4>PHx was performed on C57BL/6 mice lacking GHR (Ghr&lt;sup>-/-&lt;/sup> ), disabled for all GH-dependent Janus kinase 2 signaling (Box1&lt;sup>-/-&lt;/sup> ), or lacking only GH-dependent signal transducer and activator of transcription 5 (STAT5) signaling (Ghr391&lt;sup>-/-&lt;/sup> ), and wild-type littermates. C57BL/6 Ghr&lt;sup>-/-&lt;/sup> mice showed striking mortality within 48 hours after PHx, whereas Box1&lt;sup>-/-&lt;/sup> or Ghr391&lt;sup>-/-&lt;/sup> mice survived with normal liver regeneration. Ghr&lt;sup>-/-&lt;/sup> mortality was associ</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Feb</publication><modification>2026-05-08T15:20:06.634Z</modification><creation>2021-03-05T08:58:47Z</creation></dates><accession>S-EPMC7894545</accession><cross_references><pubmed>32342533</pubmed><doi>10.1002/hep.31297</doi></cross_references></HashMap>