ArticleMolecular and cellular biology2006
AML1/RUNX1 phosphorylation by cyclin-dependent kinases regulates the degradation of AML1/RUNX1 by the anaphase-promoting complex.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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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
49 citing papers in PubMed, 80 citations in OpenAlex.
- Application of a high-throughput swarm-based deep neural network Algorithm reveals SPAG5 downregulation as a potential therapeutic target in adult AML.Functional & integrative genomics · 2025Article
- Cyclin-dependent kinases (CDKs) are key genes regulating early development of Neptunea arthritica cumingii: evidence from comparative transcriptome and proteome analyses.BMC genomics · 2024Article
- CDK9 phosphorylates RUNX1 to promote megakaryocytic fate in megakaryocytic-erythroid progenitors.Blood · 2024Article
- Pharmacological inhibition of RAS overcomes FLT3 inhibitor resistance in FLT3-ITD+ AML through AP-1 and RUNX1.iScience · 2024Article
- CDK6 inhibits de novo lipogenesis in white adipose tissues but not in the liver.Nature communications · 2024Article
- CDK6 is essential for mesenchymal stem cell proliferation and adipocyte differentiation.Frontiers in molecular biosciences · 2023Article
- Heterogeneous nuclear ribonucleoprotein K is overexpressed in acute myeloid leukemia and causes myeloproliferation in mice via alteredNAR cancer · 2022Article
- CDC20 in and out of mitosis: a prognostic factor and therapeutic target in hematological malignancies.Journal of experimental & clinical cancer research : CR · 2022Review
- Insufficiency of FZR1 disturbs HSC quiescence by inhibiting ubiquitin-dependent degradation of RUNX1 in aplastic anemia.Leukemia · 2022Article
- Restoring RUNX1 deficiency in RUNX1 familial platelet disorder by inhibiting its degradation.Blood advances · 2021Article
- RUNX1-205, a novel splice variant of the human RUNX1 gene, has blockage effect on mesoderm-hemogenesis transition and promotion effect during the late stage of hematopoiesis.Journal of molecular cell biology · 2020Article
- RUNX1 Dosage in Development and Cancer.Molecules and cells · 2020Review
- PAK4 phosphorylating RUNX1 promotes ERα-positive breast cancer-induced osteolytic bone destruction.International journal of biological sciences · 2020Article
- CDK6 inhibits white to beige fat transition by suppressing RUNX1.Nature communications · 2018Article
- The ubiquitin ligase STUB1 regulates stability and activity of RUNX1 and RUNX1-RUNX1T1.The Journal of biological chemistry · 2017Article
- Aurora kinase-induced phosphorylation excludes transcription factor RUNX from the chromatin to facilitate proper mitotic progression.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- CDK6-mediated repression of CD25 is required for induction and maintenance of Notch1-induced T-cell acute lymphoblastic leukemia.Leukemia · 2016Article
- Runx1 Phosphorylation by Src Increases Trans-activation via Augmented Stability, Reduced Histone Deacetylase (HDAC) Binding, and Increased DNA Affinity, and Activated Runx1 Favors Granulopoiesis.The Journal of biological chemistry · 2016Article
- Loss of RUNX1/AML1 arginine-methylation impairs peripheral T cell homeostasis.British journal of haematology · 2015Article
- Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
AML1 (RUNX1) regulates hematopoiesis, angiogenesis, muscle function, and neurogenesis. Previous studies have shown that phosphorylation of AML1, particularly at serines 276 and 303, affects its transcriptional activation. Here, we report that phosphorylation of AML1 serines 276 and 303 can be blocked in vivo by inhibitors of the cyclin-dependent kinases (CDKs) Cdk1 and Cdk2. Furthermore, these residues can be phosphorylated in vitro by purified Cdk1/cyclin B and Cdk2/cyclin A. Mutant AML1 protein which cannot be phosphorylated at these sites (AML1-4A) is more stable than wild-type AML1. AML-4A is resistant to degradation mediated by Cdc20, one of the substrate-targeting subunits of the anaphase-promoting complex (APC). However, Cdh1, another targeting subunit used by the APC, can mediate the degradation of AML1-4A. A phospho-mimic protein, AML1-4D, can be targeted by Cdc20 or Cdh1. These observations suggest that both Cdc20 and Cdh1 can target AML1 for degradation by the APC but that AML1 phosphorylation may affect degradation mediated by Cdc20-APC to a greater degree.
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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.