ArticleMolecular immunology2020
Death associated protein kinase 2 suppresses T-B interactions and GC formation.
Article in Molecular immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.
- The role of DAPK2 as a key regulatory element in various human cancers: a systematic review.Molecular biology reports · 2024Pooled it
- Integrative Molecular Analyses of Inflammatory and Autoimmune Signals in Cardiac Sarcoidosis.Circulation · 2026Article
- High-dose intravenous BCG vaccination induces enhanced immune signaling in the airways.Science advances · 2025Article
- Impact of preweaning vaccination on host gene expression and antibody titers in healthy beef calves.Frontiers in veterinary science · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Germinal center (GC) formation is a critical step during T-dependent humoral immune responses. We report Death Associated Protein Kinase 2, a serine/threonine kinase, is rapidly induced in T cells following activation and plays an inhibitory role in T cell-mediated help for the GC formation. Specifically, T cells deficient in Dapk2 have an increased ability to physically conjugate with antigen-presenting B cells and to promote GC formation. However, Dapk2 does not regulate T cell receptor signaling strength and does not influence cytokine-driven T-cell subset polarization. Instead, Dapk2 dampens mTORC1 activities by associating with Raptor. Silencing of Raptor rescues defects observed with the Dapk2 insufficiency. Our study thus identifies Dapk2 as a new kinase likely involved in negative regulation of contact-dependent help delivery to B cells and GC formation.
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Registered trials
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