<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Bridgewater LC</submitter><funding>National Institute of Arthritis and Musculoskeletal and Skin Diseases</funding><funding>NIAMS NIH HHS</funding><pagination>125492</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3863484</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>2013</volume><pubmed_abstract>We recently reported a novel form of BMP2, designated nBMP2, which is translated from an alternative downstream start codon and is localized to the nucleus rather than secreted from the cell. To examine the function of nBMP2 in the nucleus, we engineered a gene-targeted mutant mouse model (nBmp2NLS(tm)) in which nBMP2 cannot be translocated to the nucleus. Immunohistochemistry demonstrated the presence of nBMP2 staining in the myonuclei of wild type but not mutant skeletal muscle. The nBmp2NLS(tm) mouse exhibits altered function of skeletal muscle as demonstrated by a significant increase in the time required for relaxation following a stimulated twitch contraction. Force frequency analysis showed elevated force production in mutant muscles compared to controls from 10 to 60 Hz stimulation</pubmed_abstract><journal>BioMed research international</journal><pubmed_title>A novel bone morphogenetic protein 2 mutant mouse, nBmp2NLS(tm), displays impaired intracellular Ca2+ handling in skeletal muscle.</pubmed_title><pmcid>PMC3863484</pmcid><funding_grant_id>AR48839</funding_grant_id><funding_grant_id>R01 AR048839</funding_grant_id><pubmed_authors>Hancock CR</pubmed_authors><pubmed_authors>Bridgewater LC</pubmed_authors><pubmed_authors>Dean SA</pubmed_authors><pubmed_authors>Dhunghel S</pubmed_authors><pubmed_authors>Holden DN</pubmed_authors><pubmed_authors>Steed KS</pubmed_authors><pubmed_authors>Evanson BG</pubmed_authors><pubmed_authors>Whitt ME</pubmed_authors><pubmed_authors>Adam MM</pubmed_authors><pubmed_authors>Schmidt AD</pubmed_authors><pubmed_authors>Loganathan SK</pubmed_authors><pubmed_authors>Nichols CA</pubmed_authors><pubmed_authors>Mayo JL</pubmed_authors><pubmed_authors>Barrow JR</pubmed_authors><pubmed_authors>Yates JD</pubmed_authors><pubmed_authors>Fox CL</pubmed_authors></additional><is_claimable>false</is_claimable><name>A novel bone morphogenetic protein 2 mutant mouse, nBmp2NLS(tm), displays impaired intracellular Ca2+ handling in skeletal muscle.</name><description>We recently reported a novel form of BMP2, designated nBMP2, which is translated from an alternative downstream start codon and is localized to the nucleus rather than secreted from the cell. To examine the function of nBMP2 in the nucleus, we engineered a gene-targeted mutant mouse model (nBmp2NLS(tm)) in which nBMP2 cannot be translocated to the nucleus. Immunohistochemistry demonstrated the presence of nBMP2 staining in the myonuclei of wild type but not mutant skeletal muscle. The nBmp2NLS(tm) mouse exhibits altered function of skeletal muscle as demonstrated by a significant increase in the time required for relaxation following a stimulated twitch contraction. Force frequency analysis showed elevated force production in mutant muscles compared to controls from 10 to 60 Hz stimulation</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013</publication><modification>2025-04-26T05:47:38.507Z</modification><creation>2019-03-27T01:18:28Z</creation></dates><accession>S-EPMC3863484</accession><cross_references><pubmed>24369527</pubmed><doi>10.1155/2013/125492</doi></cross_references></HashMap>