FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2012121717> ?p ?o ?g. }

• W2012121717 endingPage "217" @default.
• W2012121717 startingPage "204" @default.
• W2012121717 abstract "BACKGROUND Hypertrophic cardiomyopathy, characterized by thickened ventricular walls and reduced ventricular chamber volume, is a common cause of sudden cardiac death in young people. Most inherited forms result from mutations in genes encoding sarcomeric proteins. METHODS Histologic analysis identified embryonic cardiac hypertrophy in dark-like mutant mice. BrdU analysis was performed to measure proliferation and cardiomyocytes were isolated to measure cell size. The dark-like mutation was identified by positional cloning. RESULTS The dark-like mutation causes cardiomyocyte hypertrophy due to loss-of-function of peptidase d (Pepd), which encodes prolidase, a cytosolic enzyme that recycles proline for collagen re-synthesis. Prolidase deficiency is a rare autosomal recessive disease in humans with a broad phenotypic spectrum not reported to include heart defects, but a conserved role for prolidase in heart development was confirmed by morpholino knockdown in zebrafish. We tested the hypothesis that loss of prolidase function disrupts collagen-mediated integrin signaling and determined that the levels of several key integrin transducers were reduced in the hearts of dark-like mutant embryos. CONCLUSIONS This work identifies dark-like mice as a model of prolidase deficiency that will be valuable for studying the role of proline metabolism in normal physiology and disease processes, and suggests that integrin signaling may regulate the onset of hypertrophic cardiac growth. Birth Defects Research (Part A) 2011. © 2011 Wiley-Liss, Inc." @default.
• W2012121717 created "2016-06-24" @default.
• W2012121717 creator A5003530093 @default.
• W2012121717 creator A5019247983 @default.
• W2012121717 creator A5021584710 @default.
• W2012121717 creator A5023344925 @default.
• W2012121717 creator A5025148055 @default.
• W2012121717 creator A5041646089 @default.
• W2012121717 creator A5062364054 @default.
• W2012121717 date "2011-04-01" @default.
• W2012121717 modified "2023-10-16" @default.
• W2012121717 title "Developmental cardiac hypertrophy in a mouse model of prolidase deficiency" @default.
• W2012121717 cites W1896880720 @default.
• W2012121717 cites W1966021507 @default.
• W2012121717 cites W1967172937 @default.
• W2012121717 cites W1970277970 @default.
• W2012121717 cites W1970917173 @default.
• W2012121717 cites W1971902403 @default.
• W2012121717 cites W1972374716 @default.
• W2012121717 cites W1975240020 @default.
• W2012121717 cites W1998493095 @default.
• W2012121717 cites W2003035943 @default.
• W2012121717 cites W2006319239 @default.
• W2012121717 cites W2007521546 @default.
• W2012121717 cites W2016156470 @default.
• W2012121717 cites W2028179994 @default.
• W2012121717 cites W2038768348 @default.
• W2012121717 cites W2039922719 @default.
• W2012121717 cites W2042249618 @default.
• W2012121717 cites W2043168185 @default.
• W2012121717 cites W2046269659 @default.
• W2012121717 cites W2049435445 @default.
• W2012121717 cites W2051049433 @default.
• W2012121717 cites W2057516068 @default.
• W2012121717 cites W2059348822 @default.
• W2012121717 cites W2062372050 @default.
• W2012121717 cites W2065417808 @default.
• W2012121717 cites W2067837318 @default.
• W2012121717 cites W2068755144 @default.
• W2012121717 cites W2070175168 @default.
• W2012121717 cites W2078503152 @default.
• W2012121717 cites W2080622890 @default.
• W2012121717 cites W2103751591 @default.
• W2012121717 cites W2107277218 @default.
• W2012121717 cites W2116960426 @default.
• W2012121717 cites W2117914440 @default.
• W2012121717 cites W2118221757 @default.
• W2012121717 cites W2133844804 @default.
• W2012121717 cites W2139442812 @default.
• W2012121717 cites W2139618367 @default.
• W2012121717 cites W2143188350 @default.
• W2012121717 cites W2147543192 @default.
• W2012121717 cites W2149422196 @default.
• W2012121717 cites W2150527694 @default.
• W2012121717 cites W2167880464 @default.
• W2012121717 cites W2171908036 @default.
• W2012121717 cites W2179216392 @default.
• W2012121717 cites W2298596478 @default.
• W2012121717 cites W2326160676 @default.
• W2012121717 doi "https://doi.org/10.1002/bdra.20789" @default.
• W2012121717 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21472842" @default.
• W2012121717 hasPublicationYear "2011" @default.
• W2012121717 type Work @default.
• W2012121717 sameAs 2012121717 @default.
• W2012121717 citedByCount "7" @default.
• W2012121717 countsByYear W20121217172014 @default.
• W2012121717 countsByYear W20121217172015 @default.
• W2012121717 countsByYear W20121217172019 @default.
• W2012121717 countsByYear W20121217172020 @default.
• W2012121717 countsByYear W20121217172021 @default.
• W2012121717 crossrefType "journal-article" @default.
• W2012121717 hasAuthorship W2012121717A5003530093 @default.
• W2012121717 hasAuthorship W2012121717A5019247983 @default.
• W2012121717 hasAuthorship W2012121717A5021584710 @default.
• W2012121717 hasAuthorship W2012121717A5023344925 @default.
• W2012121717 hasAuthorship W2012121717A5025148055 @default.
• W2012121717 hasAuthorship W2012121717A5041646089 @default.
• W2012121717 hasAuthorship W2012121717A5062364054 @default.
• W2012121717 hasConcept C104317684 @default.
• W2012121717 hasConcept C126322002 @default.
• W2012121717 hasConcept C127716648 @default.
• W2012121717 hasConcept C134018914 @default.
• W2012121717 hasConcept C136571751 @default.
• W2012121717 hasConcept C143065580 @default.
• W2012121717 hasConcept C167414201 @default.
• W2012121717 hasConcept C173396325 @default.
• W2012121717 hasConcept C2776878037 @default.
• W2012121717 hasConcept C2778198053 @default.
• W2012121717 hasConcept C2778797674 @default.
• W2012121717 hasConcept C2780185194 @default.
• W2012121717 hasConcept C501734568 @default.
• W2012121717 hasConcept C54355233 @default.
• W2012121717 hasConcept C55493867 @default.
• W2012121717 hasConcept C71924100 @default.
• W2012121717 hasConcept C86803240 @default.
• W2012121717 hasConcept C95444343 @default.
• W2012121717 hasConceptScore W2012121717C104317684 @default.
• W2012121717 hasConceptScore W2012121717C126322002 @default.

• next