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1. Structure, regulation, and (patho-)physiological functions of the stress-induced protein kinase CK1 delta (CSNK1D).

Author

Xu P, Ianes C, Gärtner F, Liu C, Burster T, Bakulev V, Rachidi N, Knippschild U, and Bischof J

Subjects
Animals, Casein Kinase Idelta antagonists & inhibitors, Casein Kinase Idelta genetics, Drug Delivery Systems methods, Humans, Isoenzymes antagonists & inhibitors, Isoenzymes chemistry, Isoenzymes genetics, Isoenzymes metabolism, Neoplasm Proteins antagonists & inhibitors, Neoplasm Proteins genetics, Neoplasms drug therapy, Neoplasms genetics, Neoplasms pathology, Structure-Activity Relationship, Casein Kinase Idelta chemistry, Casein Kinase Idelta metabolism, Neoplasm Proteins metabolism, Neoplasms enzymology, Signal Transduction
Abstract

Members of the highly conserved pleiotropic CK1 family of serine/threonine-specific kinases are tightly regulated in the cell and play crucial regulatory roles in multiple cellular processes from protozoa to human. Since their dysregulation as well as mutations within their coding regions contribute to the development of various different pathologies, including cancer and neurodegenerative diseases, they have become interesting new drug targets within the last decade. However, to develop optimized CK1 isoform-specific therapeutics in personalized therapy concepts, a detailed knowledge of the regulation and functions of the different CK1 isoforms, their various splice variants and orthologs is mandatory. In this review we will focus on the stress-induced CK1 isoform delta (CK1δ), thereby addressing its regulation, physiological functions, the consequences of its deregulation for the development and progression of diseases, and its potential as therapeutic drug target., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Published
2019
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2. Structure, regulation, and (patho-)physiological functions of the stress-induced protein kinase CK1 delta (CSNK1D)

Author

Xu, P., Ianes, C., Gärtner, F., Liu, C., Burster, T., Bakulev, V., Rachidi, N., Knippschild, U., and Bischof, J.

Subjects
GENETIC VARIATION, ENZYME STRUCTURE, GENETIC VARIABILITY, STRESS, ISOENZYME, NEOPLASM, CYTOSKELETON, ANTAGONISTS AND INHIBITORS, DISEASE COURSE, HIPPO SIGNALING, CHEMISTRY, GENE SEQUENCE, PHOSPHORYLATION, PRIORITY JOURNAL, GENETIC TRANSCRIPTION, WNT SIGNALING, SEQUENCE ALIGNMENT, CARCINOGENESIS, SIGNAL TRANSDUCTION, HUMAN, HUMANS, MEIOSIS, CANCER, AMINO ACID SEQUENCE, PROTEIN INTERACTION, METABOLIC DISORDER, GENETIC CODE, ENZYME SUBSTRATE, MITOSIS, CASEIN KINASE IDELTA, HEDGEHOG SIGNALING, TUMOR GROWTH, NEOPLASM PROTEINS, NEOPLASMS, SITE-SPECIFIC PHOSPHORYLATION, GENETICS, SMALL MOLECULE INHIBITOR, CIRCADIAN RHYTHM, PATHOPHYSIOLOGY, ISOENZYMES, MOLECULAR RECOGNITION, CSNK1D, METABOLISM, DNA DAMAGE, DRUG DELIVERY SYSTEMS, POLYADENYLATION, CASEIN KINASE 1, NONHUMAN, REVIEW, CELL CYCLE, CSNK1D GENE, STRUCTURE-ACTIVITY RELATIONSHIP, WNT SIGNALING PATHWAY, P53, PROTEIN TARGETING, ANIMALS, ANIMAL, ENZYME REGULATION, PATHOLOGY, RNA FOLDING, HEDGEHOG PATHWAY, TUMOR PROTEIN, PROCEDURES, DRUG DEPENDENCE, DRUG DELIVERY SYSTEM, STRUCTURE ACTIVITY RELATION, STRESS-INDUCED KINASE, CELL STRESS, CELLULAR DISTRIBUTION, ENZYMOLOGY
Abstract

Members of the highly conserved pleiotropic CK1 family of serine/threonine-specific kinases are tightly regulated in the cell and play crucial regulatory roles in multiple cellular processes from protozoa to human. Since their dysregulation as well as mutations within their coding regions contribute to the development of various different pathologies, including cancer and neurodegenerative diseases, they have become interesting new drug targets within the last decade. However, to develop optimized CK1 isoform-specific therapeutics in personalized therapy concepts, a detailed knowledge of the regulation and functions of the different CK1 isoforms, their various splice variants and orthologs is mandatory. In this review we will focus on the stress-induced CK1 isoform delta (CK1δ), thereby addressing its regulation, physiological functions, the consequences of its deregulation for the development and progression of diseases, and its potential as therapeutic drug target. © 2019 Elsevier B.V.

Published
2019

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