The effect of CK2beta on the activity of CK2alpha and other protein kinases that can bind this regulatory subunit is not fully understood. In an attempt to improve our understanding of this effect, chimeras of CK2alpha and CK1alpha have been constructed. These chimeras contain different portions of the CK2alpha amino terminal region that are involved in the interaction with CK2beta to form CK2 tetramers. In the case of chimeras 1 and 2, the portions of CK2alpha replace the corresponding segments of CK1alpha. In the case of chimera 3, the fragment of CK2alpha is added to the whole CK1alpha molecule with the exception of the initial methionine. Chimera 3 has 8% of the activity of CK1alphaWT, while chimeras 1 and 2 are 3 orders of magnitude less active than CK1alphaWT. All three chimeras bind tightly to CK2beta, but only chimeras 1 and 2 are significantly stimulated in their capacity to phosphorylate casein and canonical peptide substrates by addition of the regulatory subunit. No stimulation was observed with phosvitin or non-canonical peptides derived from beta-catenin. CK2beta protects chimeras 1 and 2 from thermal inactivation. Chimera 2 can phosphorylate CK2beta and autophosphorylate; however, salt concentrations above 150 mM NaCl eliminate the phosphorylation of CK2beta but not the autophosphorylation of chimera 2. Similarly, high salt decrease the stimulatory effect of CK2beta on the phosphorylation of casein.
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http://dx.doi.org/10.1007/s11010-008-9825-2 | DOI Listing |
Diabetol Int
January 2025
Division of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, 7-5-2, Kusunoki-cho, Chuo-ku, Kobe, 650-0017 Japan.
Unlabelled: Endoplasmic reticulum (ER) stress due to obesity or systemic insulin resistance is an important pathogenic factor that could lead to pancreatic β-cell failure. We have previously reported that CCAAT/enhancer-binding protein β (C/EBPβ) is highly induced by ER stress in pancreatic β cells. Moreover, its accumulation hampers the response of these cells to ER stress by inhibiting the induction of the molecular chaperone 78 kDa glucose-regulated protein (GRP78).
View Article and Find Full Text PDFChemMedChem
January 2025
Université Claude Bernard Lyon 1: Universite Claude Bernard Lyon 1, Centre de Recherche en Cancérologie de Lyon, FRANCE.
The serine/threonine protein kinase CK2, a tetramer composed of a regulatory dimer (CK2β2) bound to two catalytic subunits CK2α, is a well-established therapeutic target for various pathologies, including cancer and viral infections. Several types of CK2 inhibitors have been developed, including inhibitors that bind to the catalytic ATP-site, bivalent inhibitors that occupy both the CK2α ATP-site and the αD pocket, and inhibitors that target the CK2α/CK2β interface. Interestingly, the bivalent inhibitor AB668 shares a similar chemical structure with the interface inhibitor CCH507.
View Article and Find Full Text PDFMolecules
December 2024
Institut für Pharmazeutische und Medizinische Chemie, Universität Münster, Corrensstraße 48, D-48149 Münster, Germany.
Cancers (Basel)
July 2024
College of Pharmacy, Xavier University of Louisiana, New Orleans, LA 70125, USA.
Aberrant estrogen receptor (ERα) signaling mediates detrimental effects of tamoxifen including drug resistance and endometrial hyperplasia. ERα36, an alternative isoform of ERα, contributes to these effects. We have demonstrated that CK2 modulates ERα expression and function in breast cancer (BCa).
View Article and Find Full Text PDFJ Trace Elem Med Biol
December 2024
School of Science, Western Sydney University, Locked Bag 1797, Penrith, NSW 2751, Australia. Electronic address:
Background: Zinc transport proteins (ZIP and ZnT), metallothioneins (MT) and protein kinase CK2 are involved in dysregulation of zinc homeostasis in breast and prostate cancer cells. Following up our previous research, we targeted ZIP12, ZnT1, MT2A and CK2 in this study by investigating their expression levels and protein localisation.
Methods: Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and immunofluorescence confocal microscopy were employed to quantify the expression of ZIP12, ZnT1, MT2A and CK2 subunits in a panel of breast and prostate cell lines without or with extracellular zinc exposure.
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