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Casein kinase II, glycogen synthase kinase-3, and Ikaros mediated regulation of leukemia has been summarized. (Review)
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Our results showcase the potentially valuable functional impact of microRNAs in regulating GG related epilepsy. As CK-2alpha inhibition enhances miR-217 expression, disrupting the miR-217-CK-2alpha interplay through CK-2alpha inhibitors might represent a novel therapeutic strategies aimed at LEAT.
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The results suggest that CK2alpha promotes migration and invasion of clear cell renal cell carcinoma and therefore could serve as a novel prognostic biomarker and molecular therapeutic target in this type of cancer.
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The newly designed casein kinase 2 (CK2) Inhibitors were screened on one lung cancer cell line A549, showing low micromolar anti-proliferative activity.
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CK2 governs the molecular decision between encephalitogenic TH17 cells and protective Treg cells development.
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Data suggest that casein kinase 2 (CK2) inhibition is a promising approach to blocking beta-catenin in MPNST cells, although combinatorial therapies may be required for maximal efficacy.
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Results provide evidence that CK2A is critical fro RSV virus replication in human cells.
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Vascular smooth muscle protein kinase CK2 inhibition suppresses neointima formation via a proline-rich homeodomain-dependent mechanism.
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we have identified kinases, particularly CK2, associated with the autocrine malignant cell network that may play a central role in sustaining the cytokine network and/or mediating its effects in ovarian cancer.
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CK2 and AKT display a high degree of cross-regulation of their respective functions, both directly, through physical interaction and phosphorylation, and indirectly, through an intense cross-talk of key downstream effectors, ultimately leading to sustained AKT activation. (Review)
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Phosphorylation of Ikaros by CK2 impairs Ikaros DNA-binding ability, as well as Ikaros ability to regulate gene expression and function as a tumor suppressor in leukemia. (Review)
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data implicate CK2 as a regulator of the Th17/Treg axis and Th17 cell maturation and suggest that CK2 could be targeted for the treatment of Th17 cell-driven autoimmune disorders.
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This study demonstrates that CSNK2A1 and SIRT6 are indicators of poor prognosis for breast carcinomas and that CSNK2A1-mediated phosphorylation of SIRT6 might be involved in the progression of breast carcinoma.
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Our results disclose a novel interplay between ubiquitin- and phosphorylation-dependent signalling, and represent the first report of a regulatory mechanism for UIM-dependent function. They also suggest that CK2 inhibitors could release the full neuroprotective potential of HSJ1, and deserve future interest as therapeutic strategies for neurodegenerative disease.
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CK2 inhibition in monocyte-derived dendritic cells led to an enhanced Th2 polarization in the absence of contact sensitizer stimulation.
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In the present work we have shown a key role for protein kinase CK2 in promoting LSC survival through the modulation of the STAT3, NF-kappaB and AKT/FOXO signaling pathways. We have also shown that CK2 inactivation makes LSCs more sensitive to the chemotherapeutic drug doxorubicin.
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our findings establish an important regulatory role of CK2alpha on BMI1 phosphorylation and stability and implicate the CK2alpha/BMI1 axis in ovarian cancer.
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The lack of intermediate species of CK2 alpha2beta2 in solution suggests that the holoenzyme is a strong/stable multimeric complex that does not spontaneously dissociate; a considerable amount of monomer, the active form of CK2, is present in low ionic strength solutions. Multimer assembly appears driven by electrostatic interactions between the CK2alpha P+1 loop and the CK2beta acidic loop.
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These data support a role for casein kinase 2 in regulation of protein synthesis by downregulating stress granule formation through G3BP1.
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The invasion and migration of A549 cells were significantly inhibited after the knockdown of CK2alpha expression.
