<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chen HH</submitter><funding>National Science and Technology Council</funding><pagination>2559-2573</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11634477</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(6)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Nuclear receptor interaction protein (NRIP) is versatile and engages with various proteins to execute its diverse biological function. NRIP deficiency was reported to cause small myofibre size in adult muscle regeneration, indicating a crucial role of NRIP in myoblast fusion.&lt;h4>Methods&lt;/h4>The colocalization and interaction of NRIP with actin were investigated by immunofluorescence and immunoprecipitation assay, respectively. The participation of NRIP in myoblast fusion was demonstrated by cell fusion assay and time-lapse microscopy. The NRIP mutants were generated for mechanism study in NRIP-null C2C12 (termed KO19) cells and muscle-specific NRIP knockout (NRIP cKO) mice. A GEO profile database was used to analyse NRIP expression in Duchenne muscular dystrophy (DMD) pa</pubmed_abstract><journal>Journal of cachexia, sarcopenia and muscle</journal><pubmed_title>The Innovative Role of Nuclear Receptor Interaction Protein in Orchestrating Invadosome Formation for Myoblast Fusion.</pubmed_title><pmcid>PMC11634477</pmcid><funding_grant_id>MOST 111-2320-B-002-077-MY3</funding_grant_id><funding_grant_id>MOST 110-2320-B-002-052-MY3</funding_grant_id><funding_grant_id>MOST 104-2320-B-002-053-MY3</funding_grant_id><funding_grant_id>MOST 107‐2320‐B‐002‐012‐MY3</funding_grant_id><funding_grant_id>MOST 107-2320-B-002-012-MY3</funding_grant_id><funding_grant_id>MOST 110‐2320‐B‐002‐052‐MY3</funding_grant_id><funding_grant_id>MOST 111‐2320‐B‐002‐077‐MY3</funding_grant_id><funding_grant_id>National Health Research Institute</funding_grant_id><funding_grant_id>MOST 104‐2320‐B‐002‐053‐MY3</funding_grant_id><funding_grant_id>NHRI-105-1053ISI</funding_grant_id><funding_grant_id>NHRI‐105‐1053ISI</funding_grant_id><pubmed_authors>Chen SL</pubmed_authors><pubmed_authors>Huang YH</pubmed_authors><pubmed_authors>Hsu WE</pubmed_authors><pubmed_authors>Tsai LK</pubmed_authors><pubmed_authors>Tsao YP</pubmed_authors><pubmed_authors>Chen HH</pubmed_authors><pubmed_authors>Lai HJ</pubmed_authors><pubmed_authors>Han YJ</pubmed_authors><pubmed_authors>Liu YH</pubmed_authors><pubmed_authors>Huang HP</pubmed_authors><pubmed_authors>Lin CY</pubmed_authors></additional><is_claimable>false</is_claimable><name>The Innovative Role of Nuclear Receptor Interaction Protein in Orchestrating Invadosome Formation for Myoblast Fusion.</name><description>&lt;h4>Background&lt;/h4>Nuclear receptor interaction protein (NRIP) is versatile and engages with various proteins to execute its diverse biological function. NRIP deficiency was reported to cause small myofibre size in adult muscle regeneration, indicating a crucial role of NRIP in myoblast fusion.&lt;h4>Methods&lt;/h4>The colocalization and interaction of NRIP with actin were investigated by immunofluorescence and immunoprecipitation assay, respectively. The participation of NRIP in myoblast fusion was demonstrated by cell fusion assay and time-lapse microscopy. The NRIP mutants were generated for mechanism study in NRIP-null C2C12 (termed KO19) cells and muscle-specific NRIP knockout (NRIP cKO) mice. A GEO profile database was used to analyse NRIP expression in Duchenne muscular dystrophy (DMD) pa</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Dec</publication><modification>2026-06-03T00:55:15.4Z</modification><creation>2025-04-06T15:09:17.119Z</creation></dates><accession>S-EPMC11634477</accession><cross_references><pubmed>39323088</pubmed><doi>10.1002/jcsm.13598</doi></cross_references></HashMap>