ArticleScience signaling2018
The DUF1669 domain of FAM83 family proteins anchor casein kinase 1 isoforms.
Article in Science signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
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Who cites it
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 157 citations in OpenAlex.
- Multiomics Data Synthesis of FAM83H in Amelogenesis Imperfecta.International dental journal · 2026Pooled it
- The Contribution of Native Protein Complexes to Targeted Protein Degradation.ACS chemical biology · 2026Article
- HMMR/RHAMM recruits SACK1D/FAM83D-CK1α complex at the mitotic spindle to control spindle alignment.iScience · 2026Article
- Phosphorylation-coupled autoregulation of TANGO1 and Sec16A maintains functional ER exit sites.Nature communications · 2025Article
- Design and Synthesis of Novel Candidate CK1δ Proteolysis Targeting Chimeras (PROTACs).Molecules (Basel, Switzerland) · 2025Article
- FAM83A is a prognostic biomarker for lung squamous cell carcinoma and correlated with immunoregulation.Scientific reports · 2025Article
- Unbiased mapping of cereblon neosubstrate landscape by high-throughput proteomics.Nature communications · 2025Article
- FNDC3B promotes gastric cancer metastasis via interacting with FAM83H and preventing its proteasomal degradation.Cellular & molecular biology letters · 2025Article
- Comprehensive analysis of FAM83B in pan-cancer and preliminary exploration in esophageal squamous cell carcinoma.Journal of molecular histology · 2025Article
- USP25-driven KIFC1 regulates MYCBP expression and promotes the progression of cervical cancer.Cell death & disease · 2025Article
- The DUF1669 domain of FAM83H is required for its localization to nuclear speckles.Scientific reports · 2025Article
- Zebrafish reveal new roles for Fam83f in hatching and the DNA damage-mediated autophagic response.Open biology · 2024Article
- The receptor protein tyrosine phosphatase PTPRK promotes intestinal repair and catalysis-independent tumour suppression.Journal of cell science · 2024Article
- Casein Kinase 1α-A Target for Prostate Cancer Therapy?Cancers · 2024Review
- A novel FAM83G variant from palmoplantar keratoderma patient disrupts WNT signalling via loss of FAM83G-CK1α interaction.Open biology · 2024Article
- Diagnostic value of immune-related biomarker FAM83A in differentiating malignant from benign pleural effusion in lung adenocarcinoma.Discover oncology · 2024Article
- FAM83B regulates mitochondrial metabolism and anti-apoptotic activity in pulmonary adenocarcinoma.Apoptosis : an international journal on programmed cell death · 2024Article
- Article
- Upregulation of FAM83F by c-Myc promotes cervical cancer growth and aerobic glycolysis via Wnt/β-catenin signaling activation.Cell death & disease · 2023Article
- CRISPR/Cas9-Induced Fam83h Knock-out Leads to Impaired Wnt/β-Catenin Pathway and Altered Expression of Tooth Mineralization Genes in Mice.Iranian journal of biotechnology · 2023Article
11 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
19 authors at 3 institutions in 1 country.
Funding
Abstract
Members of the casein kinase 1 (CK1) family of serine-threonine protein kinases are implicated in the regulation of many cellular processes, including the cell cycle, circadian rhythms, and Wnt and Hedgehog signaling. Because these kinases exhibit constitutive activity in biochemical assays, it is likely that their activity in cells is controlled by subcellular localization, interactions with inhibitory proteins, targeted degradation, or combinations of these mechanisms. We identified members of the FAM83 family of proteins as partners of CK1 in cells. All eight members of the FAM83 family (FAM83A to FAM83H) interacted with the α and α-like isoforms of CK1; FAM83A, FAM83B, FAM83E, and FAM83H also interacted with the δ and ε isoforms of CK1. We detected no interaction between any FAM83 member and the related CK1γ1, CK1γ2, and CK1γ3 isoforms. Each FAM83 protein exhibited a distinct pattern of subcellular distribution and colocalized with the CK1 isoform(s) to which it bound. The interaction of FAM83 proteins with CK1 isoforms was mediated by the conserved domain of unknown function 1669 (DUF1669) that characterizes the FAM83 family. Mutations in FAM83 proteins that prevented them from binding to CK1 interfered with the proper subcellular localization and cellular functions of both the FAM83 proteins and their CK1 binding partners. On the basis of its function, we propose that DUF1669 be renamed the polypeptide anchor of CK1 domain.
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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.