ArticleMolecular & cellular oncology
YAP enters the mTOR pathway to promote tuberous sclerosis complex.
Article in Molecular & cellular oncology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Overcoming BRAF and CDK4/6 inhibitor resistance by inhibiting MAP3K3-dependent protection against YAP lysosomal degradation.Experimental & molecular medicine · 2024Article
- Interleukin-6 mediates PSAT1 expression and serine metabolism in TSC2-deficient cells.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Single-Cell Transcriptomic Analysis Identifies a Unique Pulmonary Lymphangioleiomyomatosis Cell.American journal of respiratory and critical care medicine · 2020Article
- Phosphorylated mTOR and YAP serve as prognostic markers and therapeutic targets in gliomas.Laboratory investigation; a journal of technical methods and pathology · 2017Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in tuberous sclerosis complex 1 (TSC1) or TSC2 predispose to angiomyolipomas and lymphangioleiomyomatosis in a mTOR-dependent manner. In these mesenchymal lesions, mTOR suppresses macroautophagy-mediated lysosomal degradation of YAP, which is a transcriptional coactivator of Hippo pathway and is required for the tumorigenesis of TSC. Therapeutic applications for TSC and other diseases with dysregulated mTOR activity can be envisaged.
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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.