ArticleDevelopmental biology2015
A thioredoxin fold protein Sh3bgr regulates Enah and is necessary for proper sarcomere formation.
Article in Developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- SH3BGRL proteins are thioredoxin fold-containing actin filament pointed end capping proteins (TPECs).Scientific reports · 2026Article
- Multitrait GWAS of non-suicidal self-injury and the polygenetic effects on child psychopathology and brain structures.Cell reports. Medicine · 2025Article
- Methyltransferase METTL3 governs the modulation of SH3BGR expression through m6A methylation modification, imparting influence on apoptosis in the context of Down syndrome-associated cardiac development.Cell death discovery · 2024Article
- Construction of LncRNA-Related ceRNA Networks in Longissimus Dorsi Muscle of Jinfen White Pigs at Different Developmental Stages.Current issues in molecular biology · 2024Article
- Single-Cell Analysis Uncovers Osteoblast Factor Growth Differentiation Factor 10 as Mediator of Vascular Smooth Muscle Cell Phenotypic Modulation Associated with Plaque Rupture in Human Carotid Artery Disease.International journal of molecular sciences · 2022Article
- SH3BGRL2 exerts a dual function in breast cancer growth and metastasis and is regulated by TGF-β1.American journal of cancer research · 2020Article
- Using Whole Genome Sequencing in an African Subphenotype of Myasthenia Gravis to Generate a Pathogenetic Hypothesis.Frontiers in genetics · 2019Article
- An optimized method for cryogenic storage of Xenopus sperm to maximise the effectiveness of research using genetically altered frogs.Theriogenology · 2017Article
- Single-Cell Resolution of Temporal Gene Expression during Heart Development.Developmental cell · 2016Article
- Expression patterns of SH3BGR family members in zebrafish development.Development genes and evolution · 2016Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The sh3bgr (SH3 domain binding glutamate-rich) gene encodes a small protein containing a thioredoxin-like fold, SH3 binding domain, and glutamate-rich domain. Originally, it was suggested that increased expression of Sh3bgr may cause the cardiac phenotypes in Down's syndrome. However, it was recently reported that the overexpression of Sh3bgr did not cause any disease phenotypes in mice. In this study, we have discovered that Sh3bgr is critical for sarcomere formation in striated muscle tissues and also for heart development. Sh3bgr is strongly expressed in the developing somites and heart in Xenopus. Morpholino mediated-knockdown of sh3bgr caused severe malformation of heart tissue and disrupted segmentation of the somites. Further analysis revealed that Sh3bgr specifically localized to the Z-line in mature sarcomeres and that knockdown of Sh3bgr completely disrupted sarcomere formation in the somites. Moreover, overexpression of Sh3bgr resulted in abnormally discontinues thick firmaments in the somitic sarcomeres. We suggest that Sh3bgr does its function at least partly by regulating localization of Enah for the sarcomere formation. In addition, we provide the data supporting Sh3bgr is also necessary for proper heart development in part by affecting the Enah protein level.
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