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Rad17-S667 in the C-terminal tail is constitutively phosphorylated in vivo in a casein kinase 2-dependent manner, and the phosphorylation is important for 9-1-1 interaction
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This and previous studies have found a total of 20 CSNK2A1 variants in 28 individuals with syndromic intellectual disability. The hotspot variant c.593A>G, p.(Lys198Arg) was found in eight of 28 patients. Meanwhile, only five CSNK2B variants were identified in five individuals with neurodevelopmental disorders. We reviewed the previous literature to verify the phenotypic spectrum of CSNK2A1- and CSNK2B-related syndromes
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Mutation in CSNK2A1 cause neurodevelopmental abnormalities and dysmorphic features.
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Our findings indicate that CD163 contributes to gliomagenesis via CK2 and provides preclinical evidence that CD163 and the CD163 pathway might serve as a therapeutic target for glioma.
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Multiple conformations of kinase II subunit alpha (CK2alpha) hinge region, located near the active site, were observed during the dynamics.
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New crystal forms were exploited and one provided a crystal structure of CK2alpha2 at 1.89A resolution.
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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.
