ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Drak2 regulates the survival of activated T cells and is required for organ-specific autoimmune disease.
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 13 papers.
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Who cites it
13 citing papers in PubMed, 33 citations in OpenAlex.
- 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
- Article
- A Chemical Probe for Dark Kinase STK17B Derives Its Potency and High Selectivity through a Unique P-Loop Conformation.Journal of medicinal chemistry · 2020Article
- Drak2 is not required for tumor surveillance and suppression.International immunology · 2015Article
- 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
- Polar opposites: Erk direction of CD4 T cell subsets.Journal of immunology (Baltimore, Md. : 1950) · 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
- Regulation of the apoptosis-inducing kinase DRAK2 by cyclooxygenase-2 in colorectal cancer.British journal of cancer · 2009Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Drak2 is a serine/threonine kinase expressed in T and B cells. The absence of Drak2 renders T cells hypersensitive to suboptimal stimulation, yet Drak2(-/-) mice are enigmatically resistant to experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. We show in this study that Drak2(-/-) mice were also completely resistant to type 1 diabetes when bred to the NOD strain of mice that spontaneously develop autoimmune diabetes. However, there was not a generalized suppression of the immune system, because Drak2(-/-) mice remained susceptible to other models of autoimmunity. Adoptive transfer experiments revealed that resistance to disease was intrinsic to the T cells and was due to a loss of T cell survival under conditions of chronic autoimmune stimulation. Importantly, the absence of Drak2 did not alter the survival of naive T cells, memory T cells, or T cells responding to an acute viral infection. These experiments reveal a distinction between the immune response to persistent self-encoded molecules and transiently present infectious agents. We present a model whereby T cell survival depends on a balance of TCR and costimulatory signals to explain how the absence of Drak2 affects autoimmune disease without generalized suppression of the immune system.
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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.