ArticleCellular signalling2015
A novel crosstalk between calcium/calmodulin kinases II and IV regulates cell proliferation in myeloid leukemia cells.
Article in Cellular signalling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Rat Sarcoma Virus Family Genes in Acute Myeloid Leukemia: Pathogenetic and Clinical Implications.Biomedicines · 2025Review
- Constitutively active CaMKII Drives B lineage acute lymphoblastic leukemia/lymphoma in tp53 mutant zebrafish.PLoS genetics · 2023Article
- Cell-intrinsic factors governing quiescence vis-à-vis activation of adult hematopoietic stem cells.Molecular and cellular biochemistry · 2023Review
- Put in a "CaCells · 2022Review
- Newly characterized bovine mammary stromal region with epithelial properties supports representative epithelial outgrowth development from transplanted stem cells.Cell and tissue research · 2022Article
- Deregulated calcium signaling in blood cancer: Underlying mechanisms and therapeutic potential.Frontiers in oncology · 2022Review
- Upregulation of PNCK Promotes Metastasis and Angiogenesis via Activating NF-Journal of oncology · 2022Article
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- CaJournal of cellular immunology · 2021Article
- CaMKII Activity in the Inflammatory Response of Cardiac Diseases.International journal of molecular sciences · 2019Review
- Salinomycin triggers endoplasmic reticulum stress through ATP2A3 upregulation in PC-3 cells.BMC cancer · 2019Article
- Cross-Talk between Neurohormonal Pathways and the Immune System in Heart Failure: A Review of the Literature.International journal of molecular sciences · 2019Review
- The Multi-Functional Calcium/Calmodulin Stimulated Protein Kinase (CaMK) Family: Emerging Targets for Anti-Cancer Therapeutic Intervention.Pharmaceuticals (Basel, Switzerland) · 2019Review
- PNCK depletion inhibits proliferation and induces apoptosis of human nasopharyngeal carcinoma cellsJournal of Cancer · 2019Article
- Inhibition of CaMKK2 Enhances Fracture Healing by Stimulating Indian Hedgehog Signaling and Accelerating Endochondral Ossification.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2018Article
- A systems medicine approach for finding target proteins affecting treatment outcomes in patients with non-Hodgkin lymphoma.PloS one · 2017Article
- Inhibition of the nuclear export of p65 and IQCG in leukemogenesis by NUP98-IQCG.Frontiers of medicine · 2016Article
- DAG/PKCδ and IP3/Ca²⁺/CaMK IIβ Operate in Parallel to Each Other in PLCγ1-Driven Cell Proliferation and Migration of Human Gastric Adenocarcinoma Cells, through Akt/mTOR/S6 Pathway.International journal of molecular sciences · 2015Article
- The emerging role of CaMKII in cancer.Oncotarget · 2015Review
Corrections and comments
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Authors and funding
16 authors at 8 institutions in 2 countries.
Funding
Abstract
CaMKs link transient increases in intracellular Ca(2+) with biological processes. In myeloid leukemia cells, CaMKII, activated by the bcr-abl oncogene, promotes cell proliferation. Inhibition of CaMKII activity restricts cell proliferation, and correlates with growth arrest and differentiation. The mechanism by which the inhibition of CaMKII results in growth arrest and differentiation in myeloid leukemia cells is still unknown. We report that inhibition of CaMKII activity results in an upregulation of CaMKIV mRNA and protein in leukemia cell lines. Conversely, expression of CaMKIV inhibits autophosphorylation and activation of CaMKII, and elicits G0/G1cell cycle arrest,impairing cell proliferation. Furthermore, U937 cells expressing CaMKIV show elevated levels of Cdk inhibitors p27(kip1) and p16(ink4a) and reduced levels of cyclins A, B1 and D1. These findings were also confirmed in the K562 leukemic cell line. The relationship between CaMKII and CaMKIV is also observed in primary acute myeloid leukemia (AML) cells, and it correlates with their immunophenotypic profile. Indeed, immature MO/M1 AML showed increased CaMKIV expression and decreased pCaMKII, whereas highly differentiated M4/M5 AML showed decreased CaMKIV expression and increased pCaMKII levels. Our data reveal a novel cross-talk between CaMKII and CaMKIV and suggest that CaMKII suppresses the expression of CaMKIV to promote leukemia cell proliferation.
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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.