ArticleCell cycle (Georgetown, Tex.)2019
Ser289 phosphorylation activates both DAPK1 and DAPK2 but in response to different intracellular signaling pathways.
Article in Cell cycle (Georgetown, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.
- The role of DAPK2 as a key regulatory element in various human cancers: a systematic review.Molecular biology reports · 2024Pooled it
- Crosstalk between death-associated protein kinase 1-regulated mechanisms and dysfunctions in alzheimer's disease.Molecular biology reports · 2026Review
- Investigate of LOC101928988 Regulatory Effect on the DAPK2 Transcription in Breast Tumors.Cancer reports (Hoboken, N.J.) · 2025Article
- The microRNA-520a-3p inhibits invasion and metastasis by targeting NF-kappaB signaling pathway in non-small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Article
- The impact of DAPK1 and mTORC1 signaling association on autophagy in cancer.Molecular biology reports · 2022Review
- DAPK2 activates NF-κB through autophagy-dependent degradation of I-κBα during thyroid cancer development and progression.Annals of translational medicine · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DAPK1 and DAPK2 are calmodulin (CaM)-regulated protein kinases that share a high degree of homology in their catalytic and CaM regulatory domains. Both kinases function as tumor suppressors, and both have been implicated in autophagy regulation. Over the years, common regulatory mechanisms for the two kinases as well as kinase-specific ones have been identified. In a recent work, we revealed that DAPK2 is phosphorylated on Ser289 by the metabolic sensor AMPK, and that this phosphorylation enhances DAPK2 catalytic activity. Notably, Ser289 is conserved between DAPK1 and DAPK2, and was previously found to be phosphorylated in DAPK1 by RSK. Intriguingly, Ser289 phosphorylation was conversely reported to inhibit the pro-apoptotic activity of DAPK1 in cells. However, as the direct effect of this phosphorylation on DAPK1 catalytic activity was not tested, indirect effects were not excluded. Here, we compared Ser289 phosphorylation of the two kinases in the same cells and found that the intracellular signaling pathways that lead to Ser289 phosphorylation are mutually-exclusive and different for each kinase. In addition, we found that Ser289 phosphorylation in fact enhances DAPK1 catalytic activity, similar to the effect on DAPK2. Thus, Ser289 phosphorylation activates both DAPK1 and DAPK2, but in response to different intracellular signaling pathways.
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