ReviewFrontiers in oncology2014
The CK1 Family: Contribution to Cellular Stress Response and Its Role in Carcinogenesis.
Review in Frontiers in oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
177 citing papers in PubMed, 272 citations in OpenAlex.
- Article
- Integrated stress response activation in combination PG3 and cisplatin-treatedbioRxiv : the preprint server for biology · 2026Article
- Inhibition of inflammation and senescence with azole compound C7 enables expansion of hematopoietic stem and progenitor cells.Stem cells translational medicine · 2026Article
- Novel therapeutic targets at the crossroad between epigenetics and signal transduction pathways in B-cell lymphomas.Clinical and experimental medicine · 2026Review
- Review
- The Contribution of Native Protein Complexes to Targeted Protein Degradation.ACS chemical biology · 2026Article
- CK1-induced TERT phosphorylation mediates mitochondrial translocation to inhibit cardiomyocyte senescence and alleviate myocardial ischemia-reperfusion injury.Cell biology and toxicology · 2026Article
- Neurons with granulovacuolar degeneration bodies are resilient to tau-induced protein synthesis impairment.Science advances · 2026Article
- Development of a Chemical Probe to Enable Characterization of the Casein Kinase 1γ Subfamily.Journal of medicinal chemistry · 2026Article
- Casein kinase 1a mediates a two-step subunit remodeling mechanism to regulate the FRQ-FRH circadian clock complex.Nature communications · 2026Article
- The mitotic functions of a fission yeast CK1 enzyme are regulated by Cdk1-dependent and auto-phosphorylation.The Journal of biological chemistry · 2026Article
- Characterization of the dual functions of Leishmania CK1.2 in both the parasite and the macrophage.PloS one · 2026Article
- Impaired glycolysis-derived serine metabolism as a key driver of podocyte injury with senescence.Nature communications · 2025Article
- Design and Synthesis of Novel Candidate CK1δ Proteolysis Targeting Chimeras (PROTACs).Molecules (Basel, Switzerland) · 2025Article
- Inhibition of Casein Kinase 1International journal of molecular sciences · 2025Article
- Casein kinase I isoforms contribute to platelet activation and thrombogenesis via RIPK3-MLKL signaling.Communications biology · 2025Article
- Molecular genetic characterization ofbioRxiv : the preprint server for biology · 2025Article
- Development of a chemical probe to enable characterization of the casein kinase 1γ subfamily.bioRxiv : the preprint server for biology · 2025Article
- Autophosphorylation of conserved yeast and human casein kinase 1 isozymes regulates Elongator-dependent tRNA modifications.Nucleic acids research · 2025Article
- Phosphorylation-Dependent Stabilization of Collaborator of ARF (CARF) Suppresses Lymphoma Cell Proliferation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
117 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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 β-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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.