ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Protein kinase D orchestrates the activation of DRAK2 in response to TCR-induced Ca2+ influx and mitochondrial reactive oxygen generation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. 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, 20 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
- Genome-wide CRISPR screens in primary human natural killer cells identify countermeasures against immunosuppressive environment.Nature communications · 2026Article
- 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
- Serine/threonine kinase 17b (STK17B) signalling regulates Purkinje cell dendritic development and is altered in multiple spinocerebellar ataxias.The European journal of neuroscience · 2021Article
- Review
- 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
- Computational properties of mitochondria in T cell activation and fate.Open biology · 2016Review
- 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
- Orai1 function is essential for T cell homing to lymph nodes.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Signaling pathways in aged T cells - a reflection of T cell differentiation, cell senescence and host environment.Seminars in immunology · 2012Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
DRAK2 is a serine/threonine kinase highly enriched in lymphocytes that raises the threshold for T cell activation and maintains T cell survival following productive activation. T cells lacking DRAK2 are prone to activation under suboptimal conditions and exhibit enhanced calcium responses to AgR stimulation. Despite this, mice lacking DRAK2 are resistant to organ-specific autoimmune diseases due to defective autoreactive T cell survival. DRAK2 kinase activity is induced by AgR signaling, and in this study we show that the induction of DRAK2 activity requires Ca(2+) influx through the Ca(2+) release-activated Ca(2+) channel formed from Orai1 subunits. Blockade of DRAK2 activity with the protein kinase D (PKD) inhibitor Gö6976 or expression of a kinase-dead PKD mutant prevented activation of DRAK2, whereas a constitutively active PKD mutant promoted DRAK2 function. Knockdown of PKD in T cells strongly blocked endogenous DRAK2 activation following TCR ligation, implicating PKD as an essential intermediate in the activation of DRAK2 by Ca(2+) influx. Furthermore, we identify DRAK2 as a novel substrate of PKD, and demonstrate that DRAK2 and PKD physically interact under conditions that activate PKD. Mitochondrial generation of reactive oxygen intermediates was necessary and sufficient for DRAK2 activation in response to Ca(2+) influx. Taken together, DRAK2 and PKD form a novel signaling module that controls calcium homeostasis following T cell activation.
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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.