ArticleCell cycle (Georgetown, Tex.)2019
Fine-tuning AKT kinase activity through direct lysine methylation.
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 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- KDM4A-driven SMAD5/TGFβ axis activation as a therapeutic target in cholangiocarcinoma: mechanistic insights and translational implications.Cell & bioscience · 2025Article
- SETDB1 as a cancer target: challenges and perspectives in drug design.RSC medicinal chemistry · 2024Review
- FGFR3 Alterations in Bladder Cancer Stimulate Serine Synthesis to Induce Immune-Inert Macrophages That Suppress T-cell Recruitment and Activation.Cancer research · 2023Article
- JMJD8 Functions as a Novel AKT1 Lysine Demethylase.International journal of molecular sciences · 2022Article
- SPECC1L-deficient primary mouse embryonic palatal mesenchyme cells show speed and directionality defects.Scientific reports · 2021Article
- Aberrant JmjC domain-containing protein 8 (JMJD8) expression promotes activation of AKT and tumor epithelial-mesenchymal transition.Oncogene · 2020Article
- Loss of G-Protein Pathway Suppressor 2 Promotes Tumor Growth Through Activation of AKT Signaling.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition to the pivotal roles for histone methylation in the transcriptional regulation, emerging evidence suggests important roles for methylation of non-histone proteins in response to extra-cellular stimulatory events, with implications in governing tumorigenesis. Among the increasing list of non-histone proteins targeted for methylation, the tri-lysine-methylation modification of AKT has been recently identified to fine-tune its kinase activity and oncogenic functions. Moreover, our results implicate the histone methyltransferase SETDB1 as the methyltransferase modifying and activating AKT in a PI3K dependent manner. As such, the oncogenic function of SETDB1 in various cancers may be attributed to tumorigenesis, at least in part, through activating AKT. Therefore, targeting SETDB1, which modulates both epigenetic marks and AKT kinase activity simultaneously, is a potential strategy for novel cancer therapeutics.
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Registered trials
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