Please use this identifier to cite or link to this item: http://hdl.handle.net/10995/75259
Title: The CK1 family: Contribution to cellular stress response and its role in carcinogenesis
Authors: Knippschild, U.
Krüger, M.
Richter, J.
Xu, P.
Balbina, García-Reyes
Peifer, C.
Halekotte, J.
Bakulev, V.
Bischof, J.
Issue Date: 2014
Publisher: Frontiers Research Foundation
Citation: The CK1 family: Contribution to cellular stress response and its role in carcinogenesis / U. Knippschild, M. Krüger, J. Richter et al. // Frontiers in Oncology. — 2014. — Vol. 4 MAY. — 96.
Abstract: Members of the highly conserved and ubiquitously expressed pleiotropic CK1 family play major regulatory roles in many cellular processes including DNA-processing and repair, proliferation, cytoskeleton dynamics, vesicular trafficking, apoptosis, and cell differentiation. As a consequence of cellular stress conditions, interaction of CK1 with the mitotic spindle is manifold increased pointing to regulatory functions at the mitotic checkpoint. Furthermore, CK1 is able to alter the activity of key proteins in signal transduction and signal integration molecules. In line with this notion, CK1 is tightly connected to the regulation and degradation of ß-catenin, p53, and MDM2. Considering the importance of CK1 for accurate cell division and regulation of tumor suppressor functions, it is not surprising that mutations and alterations in the expression and/or activity of CK1 isoforms are often detected in various tumor entities including cancer of the kidney, choriocarcinomas, breast carcinomas, oral cancer, adenocarcinomas of the pancreas, and ovarian cancer. Therefore, scientific effort has enormously increased (i) to understand the regulation of CK1 and its involvement in tumorigenesis- and tumor progression-related signal transduction pathways and (ii) to develop CK1-specific inhibitors for the use in personalized therapy concepts. In this review, we summarize the current knowledge regarding CK1 regulation, function, and interaction with cellular proteins playing central roles in cellular stress-responses and carcinogenesis. © 2014 Knippschild.
Keywords: CASEIN KINASE 1
CELLULAR STRESS
CENTROSOME
DISEASE
INHIBITOR
P53
SIGNAL TRANSDUCTION
TUMORIGENESIS
ACTIVITY REGULATED CYTOSKELETON ASSOCIATED PROTEIN
BETA CATENIN
CASEIN KINASE I
CASEIN KINASE IALPHA
CASEIN KINASE IBETA
CASEIN KINASE IDELTA
CASEIN KINASE IEPSILON
CASEIN KINASE IGAMMA 1
CASEIN KINASE IGAMMA 2
CASEIN KINASE IGAMMA 3
CELL PROTEIN
CIRCADIAN RHYTHM SIGNALING PROTEIN
FIBRONECTIN
MICROTUBULE ASSOCIATED PROTEIN
PHOSPHATASE
PROTEIN KINASE
PROTEIN MDM2
PROTEIN P53
PROTEIN SERINE THREONINE KINASE
SCAFFOLD PROTEIN
SONIC HEDGEHOG PROTEIN
TUBULIN
TUMOR ANTIGEN
UNCLASSIFIED DRUG
VIRUS PROTEIN
ADENOCARCINOMA
ALCOHOLISM
APOPTOSIS
BREAST CARCINOMA
CARCINOGENESIS
CELL CYCLE REGULATION
CELL DIFFERENTIATION
CELL DIVISION
CELLULAR STRESS RESPONSE
CENTROSOME
DNA DAMAGE
ENZYME SPECIFICITY
GENE EXPRESSION
GENE MUTATION
GENETIC ANALYSIS
HIPPO SIGNALING PATHWAY
HUMAN
IMMUNE RESPONSE
INFLAMMATION
INFLAMMATORY PAIN
M PHASE CELL CYCLE CHECKPOINT
MOUTH ULCER
NUCLEOTIDE SEQUENCE
OVARY CANCER
OXIDATIVE STRESS
PROTEIN EXPRESSION
PROTEIN STRUCTURE
REVIEW
SIGNAL TRANSDUCTION
TUMOR GROWTH
WNT SIGNALING PATHWAY
URI: http://hdl.handle.net/10995/75259
Access: info:eu-repo/semantics/openAccess
SCOPUS ID: 84904662259
WOS ID: 000218397400093
PURE ID: 368507
ISSN: 2234-943X
DOI: 10.3389/fonc.2014.00096
Appears in Collections:Научные публикации, проиндексированные в SCOPUS и WoS CC

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.