ArticleInternational immunology2015
Drak2 is not required for tumor surveillance and suppression.
Article in International immunology, 2015. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Tanshinone IIA alleviates chronic endometritis via DRAK2 inhibition to restore mitochondrial function and suppress KDM3A-SLC2A3-driven NETs formation.Journal of molecular histology · 2026Article
- STK17A (DRAK1) at the crossroads of apoptosis, immunity, and cancer: Emerging roles and therapeutic opportunities.Theranostics · 2026Review
- DRAK2 regulates myosin light chain phosphorylation in T cells.Journal of cell science · 2024Article
- Evaluation of STK17B as a cancer immunotherapy target utilizing highly potent and selective small molecule inhibitors.Frontiers in immunology · 2024Article
- New insights into the characteristics of DRAK2 and its role in apoptosis: From molecular mechanisms to clinically applied potential.Frontiers in pharmacology · 2022Review
- On-chip crystallization for serial crystallography experiments and on-chip ligand-binding studies.IUCrJ · 2019Article
- STK17B promotes carcinogenesis and metastasis via AKT/GSK-3β/Snail signaling in hepatocellular carcinoma.Cell death & disease · 2018Article
- Drak2 Does Not Regulate TGF-β Signaling in T Cells.PloS one · 2015Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Drak2 is a promising therapeutic target to treat organ-specific autoimmune diseases such as type 1 diabetes and multiple sclerosis without causing generalized immune suppression. Inhibition of Drak2 may also prevent graft rejection following organ transplantation. However, Drak2 may function as a critical tumor suppressor, which would challenge the prospect of targeting Drak2 for therapeutic treatment. Thus, we examined the susceptibility of Drak2 (-/-) mice in several tumor models. We show that Drak2 is not required to prevent tumor formation in a variety of settings. Therefore, Drak2 does not function as an essential tumor suppressor in in vivo tumor models. These data further validate Drak2 as a viable therapeutic target to treat autoimmune disease and graft rejection. Importantly, these data also indicate that while Drak2 may induce apoptosis when overexpressed in cell lines, it is not an essential tumor suppressor.
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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.