ArticleAmerican journal of cancer research2020
ASK1 inhibits proliferation and migration of lung cancer cells via inactivating TAZ.
Article in American journal of cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Review
- Updated insights on ASK1 signaling: mechanisms, regulation, and therapeutic potential in diseases.Molecular and cellular biochemistry · 2025Review
- The G Protein-Coupled Receptor GPR56 Is an Inhibitory Checkpoint for NK Cell Migration.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Non-hippo kinases: indispensable roles in YAP/TAZ signaling and implications in cancer therapy.Molecular biology reports · 2023Review
- Article
- Insights into the post-translational modification and its emerging role in shaping the tumor microenvironment.Signal transduction and targeted therapy · 2021Review
- MEKK5 Interacts with and Negatively Regulates the E3 Ubiquitin Ligase NEDD4 for Mediating Lung Cancer Cell Migration.Life (Basel, Switzerland) · 2021Article
- Review
Corrections and comments
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Authors and funding
11 authors.
Funding
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Abstract
ASK1 (Apoptosis Signal-regulating Kinase 1, also MEKK5) is known to mediate cellular stress signaling pathways through activating p38 kinase. We here observed that ectopically expression of ASK1, but not its kinase-dead mutant, impaired cell proliferation and migration in lung cancer A549 and NCI-H1975 cells. To our surprise, this inhibitory effect of ASK1 is independent on activation of p38 kinase. We further discovered that ASK1 interacts with the WW domain of YAP and TAZ (also WWTR1) that are transcriptional co-activators and the Hippo signaling effectors. Overexpression of wild type ASK1, but not the kinase-dead mutant, in the lung cancer cells down-regulated the expression of the YAP/TAZ target genes
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Identifiers
33042617PMC7539782What OpenQuestion holds
Registered trials
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