ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2019
Tsg101 positively regulates physiologic-like cardiac hypertrophy through FIP3-mediated endosomal recycling of IGF-1R.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The trial behind it
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Overexpression of TSG101 causes the development of adenosquamous mammary carcinoma.Breast cancer research : BCR · 2025Article
- EHD1-dependent traffic of IGF-1 receptor to the cell surface is essential for Ewing sarcoma tumorigenesis and metastasis.Communications biology · 2023Article
- CD82 palmitoylation site mutations at Cys5+Cys74 affect EGFR internalization and metabolism through recycling pathway.Acta biochimica et biophysica Sinica · 2022Article
- Tumor susceptibility gene 101 is required for the maintenance of uterine epithelial cells during embryo implantation.Reproductive biology and endocrinology : RB&E · 2021Article
- Targets identified from exercised heart: killing multiple birds with one stone.NPJ Regenerative medicine · 2021Review
- Article
- Analysis of extracellular vesicle miRNA profiles in heart failure.Journal of cellular and molecular medicine · 2020Article
- Tsg101 positively regulates P62-Keap1-Nrf2 pathway to protect hearts against oxidative damage.Redox biology · 2020Article
- The Multifaceted Roles of the Tumor Susceptibility Gene 101 (TSG101) in Normal Development and Disease.Cancers · 2020Review
- Tumor susceptibility gene 101 ameliorates endotoxin-induced cardiac dysfunction by enhancing Parkin-mediated mitophagy.The Journal of biological chemistry · 2019Article
- Review
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
Abstract
Development of physiologic cardiac hypertrophy has primarily been ascribed to the IGF-1 and its receptor, IGF-1 receptor (IGF-1R), and subsequent activation of the protein kinase B (Akt) pathway. However, regulation of endosome-mediated recycling and degradation of IGF-1R during physiologic hypertrophy has not been investigated. In a physiologic hypertrophy model of treadmill-exercised mice, we observed that levels of tumor susceptibility gene 101 (Tsg101), a key member of the endosomal sorting complex required for transport, were dramatically elevated in the heart compared with sedentary controls. To determine the role of Tsg101 on physiologic hypertrophy, we generated a transgenic (TG) mouse model with cardiac-specific overexpression of Tsg101. These TG mice exhibited a physiologic-like cardiac hypertrophy phenotype at 8 wk evidenced by:
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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.