ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Enhanced T cell apoptosis within Drak2-deficient mice promotes resistance to autoimmunity.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 33 citations in OpenAlex.
- Genome-wide CRISPR screens in primary human natural killer cells identify countermeasures against immunosuppressive environment.Nature communications · 2026Article
- 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
- Serine/threonine kinase 17b (STK17B) signalling regulates Purkinje cell dendritic development and is altered in multiple spinocerebellar ataxias.The European journal of neuroscience · 2021Article
- A Chemical Probe for Dark Kinase STK17B Derives Its Potency and High Selectivity through a Unique P-Loop Conformation.Journal of medicinal chemistry · 2020Article
- DAP Kinase-Related Apoptosis-Inducing Protein Kinase 2 (DRAK2) Is a Key Regulator and Molecular Marker in Chronic Lymphocytic Leukemia.International journal of molecular sciences · 2020Article
- TCGA: Increased oncoprotein coding region mutations correlate with a greater expression of apoptosis-effector genes and a positive outcome for stomach adenocarcinoma.Cell cycle (Georgetown, Tex.) · 2016Article
- Drak2 Does Not Regulate TGF-β Signaling in T Cells.PloS one · 2015Article
- Modulation of T Cell Metabolism and Function through Calcium Signaling.Frontiers in immunology · 2013Review
- Loss of DRAK2 signaling enhances allogeneic transplant survival by limiting effector and memory T cell responses.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2012Article
- Protein kinase D orchestrates the activation of DRAK2 in response to TCR-induced Ca2+ influx and mitochondrial reactive oxygen generation.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Altered thymic selection and increased autoimmunity caused by ectopic expression of DRAK2 during T cell development.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Clonal expansion of T cells is vital to adaptive immunity, yet this process must be tightly controlled to prevent autoimmune disease. The serine/threonine kinase death-associated protein kinase-related apoptosis-inducing kinase 2 (DRAK2) is a negative regulator of TCR signaling and sets the threshold for the activation of naive and memory T cells and selected thymocytes. Despite enhanced T cell activation, Drak2(-/-) mice are resistant to experimental autoimmune encephalomyelitis, an autoimmune demyelinating disease that resembles multiple sclerosis. However, the basis for this autoimmune resistance is currently unknown. In this study, we show that, in the absence of DRAK2 signaling, T cells require greater tonic signaling for maintenance during clonal expansion. Following stimulation, Drak2(-/-) T cells were more sensitive to an intrinsic form of apoptosis that was prevented by CD28 ligation, homeostatic cytokines, or enforced Bcl-x(L) expression. T cell-specific Bcl-x(L) expression also restored the susceptibility of Drak2(-/-) mice to experimental autoimmune encephalomyelitis and enhanced thymic positive selection. These findings demonstrate that DRAK2 is selectively important for T cell survival and highlight the potential that DRAK2 blockade may lead to permanent autoimmune T cell destruction via intrinsic apoptosis pathways.
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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.