ArticleBlood2011
A CK2-dependent mechanism for activation of the JAK-STAT signaling pathway.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 2 of them syntheses that pooled it.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
71 citing papers in PubMed, 2 syntheses or guidelines pooled it, 133 citations in OpenAlex.
- Epithelial membrane protein 1 in human cancer: a potential diagnostic biomarker and therapeutic target.Biomarkers in medicine · 2024Pooled it
- CSNK2 in cancer: pathophysiology and translational applications.British journal of cancer · 2022Pooled it
- Selective Inhibition of CK2: Emerging Strategies and Future Directions.Journal of medicinal chemistry · 2026Review
- Protein Kinase CK2 Inhibition Represents a Pharmacological Chance for the Treatment of Skin Diseases.International journal of molecular sciences · 2025Review
- Article
- Mcam stabilizes a luminal progenitor-like breast cancer cell state via Ck2 control and Src/Akt/Stat3 attenuation.NPJ breast cancer · 2024Article
- The crosstalk between copper-induced oxidative stress and cuproptosis: a novel potential anticancer paradigm.Cell communication and signaling : CCS · 2024Review
- Curcumin in Cancer and Inflammation: An In-Depth Exploration of Molecular Interactions, Therapeutic Potentials, and the Role in Disease Management.International journal of molecular sciences · 2024Review
- Kinome and phosphoproteome reprogramming underlies the aberrant immune responses in critically ill COVID-19 patients.Clinical proteomics · 2024Article
- VISTA promotes the metabolism and differentiation of myeloid-derived suppressor cells by STAT3 and polyamine-dependent mechanisms.Cell reports · 2024Article
- Inhibition of CK2/ING4 Pathway Facilitates Non-Small Cell Lung Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Review
- The MEF2A transcription factor interactome in cardiomyocytes.Cell death & disease · 2023Article
- Past, Present, and a Glance into the Future of Multiple Myeloma Treatment.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Protein Kinase CK2 and Epstein-Barr Virus.Biomedicines · 2023Review
- Review
- Copper-Dependent Kinases and Their Role in Cancer Inception, Progression and Metastasis.Biomolecules · 2022Review
- CK2 and the Hallmarks of Cancer.Biomedicines · 2022Review
- The Role of Protein Kinase CK2 in Development and Disease Progression: A Critical Review.Journal of developmental biology · 2022Review
- Inhibitory Response to CK II Inhibitor Silmitasertib and CDKs Inhibitor Dinaciclib Is Related to Genetic Differences in Pancreatic Ductal Adenocarcinoma Cell Lines.International journal of molecular sciences · 2022Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
JAK-STAT signaling is involved in the regulation of cell survival, proliferation, and differentiation. JAK tyrosine kinases can be transiently activated by cytokines or growth factors in normal cells, whereas they become constitutively activated as a result of mutations that affect their function in tumors. Specifically, the JAK2V617F mutation is present in the majority of patients with myeloproliferative disorders (MPDs) and is implicated in the pathogenesis of these diseases. In the present study, we report that the kinase CK2 is a novel interaction partner of JAKs and is essential for JAK-STAT activation. We demonstrate that cytokine-induced activation of JAKs and STATs and the expression of suppressor of cytokine signaling 3 (SOCS-3), a downstream target, are inhibited by CK2 small interfering RNAs or pharmacologic inhibitors. Endogenous CK2 is associated with JAK2 and JAK1 and phosphorylates JAK2 in vitro. To extend these findings, we demonstrate that CK2 interacts with JAK2V617F and that CK2 inhibitors suppress JAK2V617F autophosphorylation and downstream signaling in HEL92.1.7 cells (HEL) and primary cells from polycythemia vera (PV) patients. Furthermore, CK2 inhibitors potently induce apoptosis of HEL cells and PV cells. Our data provide evidence for novel cross-talk between CK2 and JAK-STAT signaling, with implications for therapeutic intervention in JAK2V617F-positive MPDs.
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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.