ArticleMolecular biology of the cell1996
Modulation of myosin filament organization by C-protein family members.
Article in Molecular biology of the cell, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 62 citations in OpenAlex.
- In vitro protein expression profile of cultivated muscle cells from Labeo rohita.Scientific reports · 2025Article
- Mechanisms underlying ICU muscle wasting and effects of passive mechanical loading.Critical care (London, England) · 2012Article
- Myofibrillar protein and gene expression in acute quadriplegic myopathy.Journal of the neurological sciences · 2009Article
- The structure of isolated cardiac Myosin thick filaments from cardiac Myosin binding protein-C knockout mice.Biophysical journal · 2008Article
- PKCepsilon increases phosphorylation of the cardiac myosin binding protein C at serine 302 both in vitro and in vivo.Biochemistry · 2007Article
- Impact of post-synaptic block of neuromuscular transmission, muscle unloading and mechanical ventilation on skeletal muscle protein and mRNA expression.Pflugers Archiv : European journal of physiology · 2006Article
- Microtubule-dependent transport and organization of sarcomeric myosin during skeletal muscle differentiation.The EMBO journal · 2005Article
- Effect of MyBP-C binding to actin on contractility in heart muscle.The Journal of general physiology · 2003Article
- Dilated cardiomyopathy in homozygous myosin-binding protein-C mutant mice.The Journal of clinical investigation · 1999Article
- In vitro motility speed of slow myosin extracted from single soleus fibres from young and old rats.The Journal of physiology · 1999Article
- Assembly of thick filaments and myofibrils occurs in the absence of the myosin head.The EMBO journal · 1999Article
- A mouse model of myosin binding protein C human familial hypertrophic cardiomyopathy.The Journal of clinical investigation · 1998Article
- Molecular pathology of familial hypertrophic cardiomyopathy caused by mutations in the cardiac myosin binding protein C gene.Journal of medical genetics · 1998Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We have analyzed the interactions between two types of sarcomeric proteins: myosin heavy chain (MyHC) and members of an abundant thick filament-associated protein family (myosin-binding protein; MyBP). Previous work has demonstrated that when MyHC is transiently transfected into mammalian nonmuscle COS cells, the expressed protein forms spindle-shaped structures consisting of bundles of myosin thick filaments. Co-expression of MyHC and MyBP-C or -H modulates the MyHC structures, resulting in dramatically longer cables consisting of myosin and MyBP encircling the nucleus. Immunoelectron microscopy indicates that these cable structures are more uniform in diameter than the spindle structures consisting solely of MyHC, and that the myosin filaments are compacted in the presence of MyBP. Deletion analysis of MyBP-H indicates that cable formation is dependent on the carboxy terminal 24 amino acids. Neither the MyHC spindles nor the MyHC/MyBP cables associate with the endogenous actin cytoskeleton of the COS cell. While there is no apparent co-localization between these structures and the microtubule network, colchicine treatment of the cells promotes the formation of longer assemblages, suggesting that cytoskeletal architecture may physically impede or regulate polymer formation/extension. The data presented here contribute to a greater understanding of the interactions between the MyBP family and MyHC, and provide additional evidence for functional homology between MyBP-C and MyBP-H.
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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.