ArticleThe Journal of biological chemistry2012
STK25 protein mediates TrkA and CCM2 protein-dependent death in pediatric tumor cells of neural origin.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- STK25 Loss Augments Anti-PD-1 Therapy Efficacy by Regulating PD-L1 Stability in Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- TLR-induced STK25 activation promotes IRF5-mediated inflammation.Life science alliance · 2025Article
- Exosomal miR-4800-3p Aggravates the Progression of Hepatocellular CarcinomaFrontiers in oncology · 2022Article
- Neurotrophin Signaling in Medulloblastoma.Cancers · 2020Review
- Cerebral Cavernous Malformation Proteins in Barrier Maintenance and Regulation.International journal of molecular sciences · 2020Review
- STK25-induced inhibition of aerobic glycolysis via GOLPH3-mTOR pathway suppresses cell proliferation in colorectal cancer.Journal of experimental & clinical cancer research : CR · 2018Article
- Mammalian Sterile20-like Kinases: Signalings and Roles in Central Nervous System.Aging and disease · 2018Review
- Recent advances in cerebral cavernous malformation research.Vessel plus · 2018Article
- Microarray Analysis Reveals Increased Transcriptional Repression and Reduced Metabolic Activity but Not Major Changes in the Core Apoptotic Machinery during Maturation of Sympathetic Neurons.Frontiers in cellular neuroscience · 2016Article
- Signaling pathways and the cerebral cavernous malformations proteins: lessons from structural biology.Cellular and molecular life sciences : CMLS · 2014Review
- Cerebral cavernous malformation proteins at a glance.Journal of cell science · 2014Review
- STRIPAK complexes: structure, biological function, and involvement in human diseases.The international journal of biochemistry & cell biology · 2014Review
- Cerebral cavernous malformation is a vascular disease associated with activated RhoA signaling.Biological chemistry · 2013Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 5 countries.
Funding
Abstract
The TrkA receptor tyrosine kinase induces death in medulloblastoma cells via an interaction with the cerebral cavernous malformation 2 (CCM2) protein. We used affinity proteomics to identify the germinal center kinase class III (GCKIII) kinases STK24 and STK25 as novel CCM2 interactors. Down-modulation of STK25, but not STK24, rescued medulloblastoma cells from NGF-induced TrkA-dependent cell death, suggesting that STK25 is part of the death-signaling pathway initiated by TrkA and CCM2. CCM2 can be phosphorylated by STK25, and the kinase activity of STK25 is required for death signaling. Finally, STK25 expression in tumors is correlated with positive prognosis in neuroblastoma patients. These findings delineate a death-signaling pathway downstream of neurotrophic receptor tyrosine kinases that may provide targets for therapeutic intervention in pediatric tumors of neural origin.
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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.