| http://purl.uniprot.org/citations/37851308 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/37851308 | http://www.w3.org/2000/01/rdf-schema#comment | "M-LP/Mpv17L (Mpv17-like protein) is an atypical cyclic nucleotide phosphodiesterase (PDE) without the molecular structure characteristic of the PDE family. Deficiency of M-LP/Mpv17L in mice has been found to result in development of β-cell hyperplasia and improved glucose tolerance. Here, we report another phenotype observed in M-LP/Mpv17L-knockout (KO) mice: afferent cardiac hypertrophy. Although the hearts of M-LP/Mpv17L-KO mice did not differ in size from those of wild-type mice, there was marked narrowing of the left ventricular lumen and thickening of the ventricular wall. The diameter and cross-sectional area of cardiomyocytes in 8-month-old M-LP/Mpv17L-KO mice were increased 1.16-fold and 1.35-fold, respectively, relative to control mice, but showed no obvious abnormalities of cell structure, fibrosis or impaired cardiac function. In 80-day-old KO mice, the expression of hypertrophic marker genes, brain natriuretic peptide (BNF), actin alpha cardiac muscle 1 (ACTC1) and actin alpha 1 skeletal muscle (ACTA1), as well as the Wnt/β-catenin pathway target genes, lymphoid enhancer-binding factor-1 (LEF1), axis inhibition protein 2 (AXIN2) and transcription factor 7 (TCF7), was significantly up-regulated relative to control mice, whereas fibrosis-related genes such as fibronectin 1 (FN1) and connective tissue growth factor (CTGF) were down-regulated. Western blot analysis revealed increased phosphorylation of molecules downstream of the cAMP/PKA signaling pathway, such as β-catenin, ryanodine receptor 2 (RyR2), phospholamban (PLN) and troponin I (cTnI), as well as members of the MEK1-ERK1/2 signaling pathway, which is strongly involved in afferent cardiac hypertrophy. Taken together, these findings indicate that M-LP/Mpv17L is one of the PDEs actively functioning in the heart and that deficiency of M-LP/Mpv17L in mice promotes physiological cardiac hypertrophy."xsd:string |
| http://purl.uniprot.org/citations/37851308 | http://purl.org/dc/terms/identifier | "doi:10.1007/s11248-023-00373-7"xsd:string |
| http://purl.uniprot.org/citations/37851308 | http://purl.uniprot.org/core/author | "Yasuda T."xsd:string |
| http://purl.uniprot.org/citations/37851308 | http://purl.uniprot.org/core/author | "Ueki M."xsd:string |
| http://purl.uniprot.org/citations/37851308 | http://purl.uniprot.org/core/author | "Iida R."xsd:string |
| http://purl.uniprot.org/citations/37851308 | http://purl.uniprot.org/core/date | "2023"xsd:gYear |
| http://purl.uniprot.org/citations/37851308 | http://purl.uniprot.org/core/name | "Transgenic Res"xsd:string |
| http://purl.uniprot.org/citations/37851308 | http://purl.uniprot.org/core/pages | "575-582"xsd:string |
| http://purl.uniprot.org/citations/37851308 | http://purl.uniprot.org/core/title | "Knockout of M-LP/Mpv17L, a newly identified atypical PDE, induces physiological afferent cardiac hypertrophy in mice."xsd:string |
| http://purl.uniprot.org/citations/37851308 | http://purl.uniprot.org/core/volume | "32"xsd:string |
| http://purl.uniprot.org/citations/37851308 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/37851308 |
| http://purl.uniprot.org/citations/37851308 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/37851308 |
| http://purl.uniprot.org/uniprot/#_D3Z6M3-mappedCitation-37851308 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/37851308 |
| http://purl.uniprot.org/uniprot/#_Q8CC11-mappedCitation-37851308 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/37851308 |
| http://purl.uniprot.org/uniprot/#_Q99MS3-mappedCitation-37851308 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/37851308 |
| http://purl.uniprot.org/uniprot/Q99MS3 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/37851308 |
| http://purl.uniprot.org/uniprot/Q8CC11 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/37851308 |
| http://purl.uniprot.org/uniprot/D3Z6M3 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/37851308 |