ArticleExperimental cell research2008
Krp1 (Sarcosin) promotes lateral fusion of myofibril assembly intermediates in cultured mouse cardiomyocytes.
Article in Experimental cell research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Altered contractility, CaAmerican journal of physiology. Heart and circulatory physiology · 2023Article
- Desmin Knock-Out Cardiomyopathy: A Heart on the Verge of Metabolic Crisis.International journal of molecular sciences · 2022Article
- Molecular-scale visualization of sarcomere contraction within native cardiomyocytes.Nature communications · 2021Article
- Characterization and Comparative Transcriptomic Analysis of Skeletal Muscle in Pekin Duck at Different Growth Stages Using RNA-Seq.Animals : an open access journal from MDPI · 2021Article
- Novel KLHL26 variant associated with a familial case of Ebstein's anomaly and left ventricular noncompaction.Molecular genetics & genomic medicine · 2020Article
- Assembly and Maintenance of Sarcomere Thin Filaments and Associated Diseases.International journal of molecular sciences · 2020Review
- miR-26a-5p protects against myocardial ischemia/reperfusion injury by regulating the PTEN/PI3K/AKT signaling pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020Article
- Essential role of the zinc finger transcription factor Casz1 for mammalian cardiac morphogenesis and development.The Journal of biological chemistry · 2014Article
- Kelch proteins: emerging roles in skeletal muscle development and diseases.Skeletal muscle · 2014Review
- Identification of KLHL41 Mutations Implicates BTB-Kelch-Mediated Ubiquitination as an Alternate Pathway to Myofibrillar Disruption in Nemaline Myopathy.American journal of human genetics · 2013Article
- Breaking down protein degradation mechanisms in cardiac muscle.Trends in molecular medicine · 2013Review
- BTB-Kelch protein Krp1 regulates proliferation and differentiation of myoblasts.American journal of physiology. Cell physiology · 2011Article
- Scaffolds and chaperones in myofibril assembly: putting the striations in striated muscle.Biophysical reviews · 2011Article
- BTB-Kelch proteins and ubiquitination of kainate receptors.Advances in experimental medicine and biology · 2011Review
- Dominant mutations in KBTBD13, a member of the BTB/Kelch family, cause nemaline myopathy with cores.American journal of human genetics · 2010Article
- Novel beta-propeller of the BTB-Kelch protein Krp1 provides a binding site for Lasp-1 that is necessary for pseudopodial extension.The Journal of biological chemistry · 2009Article
- Myofibril assembly visualized by imaging N-RAP, alpha-actinin, and actin in living cardiomyocytes.Experimental cell research · 2009Article
- Expression and alternative splicing of N-RAP during mouse skeletal muscle development.Cell motility and the cytoskeleton · 2008Article
- Role of nonmuscle myosin IIB and N-RAP in cell spreading and myofibril assembly in primary mouse cardiomyocytes.Cell motility and the cytoskeleton · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Krp1, also called sarcosin, is a cardiac and skeletal muscle kelch repeat protein hypothesized to promote the assembly of myofibrils, the contractile organelles of striated muscles, through interaction with N-RAP and actin. To elucidate its role, endogenous Krp1 was studied in primary embryonic mouse cardiomyocytes. While immunofluorescence showed punctate Krp1 distribution throughout the cell, detergent extraction revealed a significant pool of Krp1 associated with cytoskeletal elements. Reduction of Krp1 expression with siRNA resulted in specific inhibition of myofibril accumulation with no effect on cell spreading. Immunostaining analysis and electron microscopy revealed that cardiomyocytes lacking Krp1 contained sarcomeric proteins with longitudinal periodicities similar to mature myofibrils, but fibrils remained thin and separated. These thin myofibrils were degraded by a scission mechanism distinct from the myofibril disassembly pathway observed during cell division in the developing heart. The data are consistent with a model in which Krp1 promotes lateral fusion of adjacent thin fibrils into mature, wide myofibrils and contribute insight into mechanisms of myofibrillogenesis and disassembly.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.