| 2001 |
Crystal structure of the human CK2 holoenzyme at 3.1 Å resolution revealed that the two regulatory (CK2β/CSNK2B) subunits form a stable dimer that links the two catalytic subunits, which make no direct contact with one another. Each catalytic subunit interacts with both regulatory chains predominantly via an extended C-terminal tail of CK2β. |
X-ray crystallography of truncated CK2 holoenzyme |
The EMBO journal |
High |
11574463
|
| 2001 |
FACT (hSpt16/SSRP1) associates with CK2 (containing the CK2β subunit) to form a UV-activated kinase complex that selectively phosphorylates p53 at Ser-392; FACT alters CK2 substrate specificity within the complex, switching preference away from casein toward p53, and this phosphorylation enhances p53 activity. |
Biochemical purification, in vitro kinase assay, functional p53 activity assay |
Molecular cell |
High |
11239457
|
| 2001 |
Bid is phosphorylated by casein kinase II (CKII, which contains CSNK2B as its regulatory subunit); phosphorylated Bid is insensitive to caspase-8 cleavage in vitro, and inhibition of CKII accelerated Fas-mediated apoptosis and Bid cleavage, whereas kinase hyperactivity delayed apoptosis. |
In vitro kinase assay, site-specific mutagenesis, caspase-8 cleavage assay, Fas apoptosis assay |
Molecular cell |
High |
11583622
|
| 1995 |
Cloning and disruption of CKB1 (the yeast ortholog of CSNK2B) demonstrated that the regulatory β subunit of CK2 is dispensable for viability, mating, and sporulation in S. cerevisiae, but strains lacking CKB1 (alone or combined with CKB2) are sensitive to NaCl and LiCl, indicating a role for the regulatory subunit in ion homeostasis. |
Gene disruption, salt sensitivity growth assays, phenotypic analysis of haploid/diploid yeast mutants |
The Journal of biological chemistry |
High |
7737972
|
| 1994 |
Cloning of CKB2 (yeast β'-subunit paralog) revealed that the β'-subunit shares a conserved CPX3C-X22-CPXC metal-binding (zinc finger) motif with other CK2β subunits. Double disruption of CKB2 with either catalytic subunit gene causes synthetic slow growth and flocculation, demonstrating that CKB2 interacts functionally with both catalytic subunits in vivo. |
Gene cloning, sequence analysis, genetic epistasis via double-mutant synthetic phenotype |
The Journal of biological chemistry |
Medium |
8027080
|
| 1996 |
CSNK2B was mapped to the class III region of the human major histocompatibility complex on chromosome 6, approximately 220 kb from known flanking genes, establishing its genomic locus. |
cDNA isolation, Northern blot, exon trapping, genomic sequencing |
Genomics |
Medium |
8812450
|
| 2013 |
Chimeric transcripts between CSNK2B and the downstream Ly6g5b gene are produced by transcription-induced chimerism and are conserved across six mammalian species; overexpression studies showed that CSNK2B, LY6G5B, and CSNK2B-LY6G5B chimeric proteins display different patterns of post-translational modifications and distinct subcellular distributions, and some chimeric transcripts encode CSNK2B proteins with an altered C-terminus that could affect substrate specificity. |
RT-PCR across six mammalian species, overexpression of tagged constructs, immunofluorescence/localization analysis |
BMC genomics |
Medium |
23521802
|
| 2014 |
CSNK2B (as the CK2 component of the PRC1-AUTS2 complex) was found to neutralize PRC1 repressive activity, allowing AUTS2-mediated recruitment of P300 and consequent gene activation in the CNS; this places CK2β within an epigenetic activation complex rather than in its canonical repressive context. |
Biochemical purification of PRC1-AUTS2 complex, ChIP-seq, conditional mouse CNS knockout |
Nature |
High |
25519132
|
| 2018 |
Knockdown of CSNK2B in neural stem cells promotes proliferation and inhibits differentiation, and alters neuronal morphology and synaptic transmission, establishing a functional role for CSNK2B in neural stem cell fate and neuronal development. |
shRNA knockdown in neural stem cells, proliferation and differentiation assays, neuronal morphology analysis, synaptic transmission measurement |
Nature communications |
Medium |
29483533
|
| 2020 |
TNFAIP1 physically interacts with CSNK2B and promotes its Cul3-mediated ubiquitin-dependent degradation, thereby attenuating CSNK2B-dependent NF-κB transactivation in hepatocellular carcinoma cells; enforced CSNK2B expression counteracts TNFAIP1's tumor-suppressive effects. |
LC-MS/MS, Co-immunoprecipitation, Western blot, dual-luciferase reporter, rescue overexpression experiments in vitro and in vivo |
EBioMedicine |
High |
31901862
|
| 2022 |
Disease-associated missense variants at Asp32 of CSNK2B (p.Asp32His and p.Asp32Asn) upregulate CSNK2B transcript and protein levels, impair the interaction of CK2β with DVL3 and β-catenin, reduce phosphorylation of β-catenin, abolish active β-catenin nuclear accumulation, and broadly dysregulate canonical Wnt signaling; whole-phosphoproteome analysis showed absence of phosphorylation of 313 putative CK2 substrates enriched in Wnt/β-catenin targets. |
Patient-derived lymphoblastoid cell lines, Co-IP, Western blot, whole-transcriptome profiling, whole-phosphoproteome mass spectrometry, immunofluorescence |
HGG advances |
High |
35571680
|
| 2023 |
CSNK2B directly interacts with IRF1 and constitutively modulates its transcriptional activity; genome-wide CUT&RUN revealed that CSNK2B broadly enhances IRF1 binding to chromatin to upregulate antiviral genes (e.g., PLAAT4/RARRES3), while its depletion causes aberrant IRF1 accumulation at AFAP1 loci. CSNK2B also mediates phosphorylation-dependent activation of the AFAP1-Src signaling axis and exerts suppressive activity against flaviviruses including dengue virus. |
Proteomics interactome screen, Co-IP, genome-wide CUT&RUN, siRNA knockdown, antiviral assays |
Nucleic acids research |
High |
37094077
|
| 2023 |
HIKER/LINC02228 lncRNA regulates erythropoiesis in Monge's disease through CSNK2B: downregulation of HIKER reduces CSNK2B expression and severely impairs erythropoiesis, while re-expression of CSNK2B on a HIKER-knockdown background rescues erythropoiesis. Pharmacological inhibition or zebrafish knockdown of CSNK2B reduces erythroid colony formation and hemoglobinization. |
RNA-Seq, lncRNA knockdown/overexpression, CSNK2B rescue overexpression, CK2 inhibitor assay, zebrafish morpholino knockdown |
The Journal of clinical investigation |
High |
37022795
|
| 2024 |
RACK1 interacts with CSNK2B and inhibits its ubiquitination-mediated degradation, stabilizing CK2β; this allows CK2 to activate the NF-κB pathway, increasing CDK4 and cyclin D3 transcription and promoting G2/M cell cycle transition in meningioma cells. |
Protein immunoprecipitation, mass spectrometry, RNA interference, transcriptome sequencing, in vivo nude mouse experiments |
Cancers |
Medium |
38398158
|
| 2021 |
CSNK2B promotes colorectal cancer cell proliferation primarily by activating the mTOR signaling pathway, as demonstrated by rescue experiments with mTOR pathway components. |
Western blot, rescue overexpression experiments, in vitro and in vivo cell viability assays |
Journal of cell communication and signaling |
Medium |
33928514
|
| 2023 |
miR-1205 directly targets the CSNK2B 3′ UTR to suppress its expression; CSNK2B in turn promotes HCC cell proliferation through a CDK4/pRb cell cycle pathway, placing CSNK2B upstream of CDK4 in this axis. |
Dual-luciferase reporter assay, western blot, rescue overexpression/knockdown in vitro and in vivo |
Technology in cancer research & treatment |
Medium |
36617978
|
| 2025 |
Pathogenic missense variants in the zinc-finger domain of CSNK2B (p.Arg111Pro, p.Cys137Phe) reduce CK2β protein stability through proteasomal and lysosomal degradation and significantly impair CK2β homodimerization, while not affecting CK2α binding; other variants (p.Asp32Asn, p.Arg86Cys) do not affect stability or CK2β/α binding, suggesting variant-class-specific mechanisms. Zinc-finger variants also alter subcellular localization of CK2β. |
Western blot, proteasome/lysosome inhibitor assays, co-immunoprecipitation for homodimerization and CK2α binding, immunofluorescence localization |
Biological chemistry |
Medium |
40317201
|
| 2023 |
Haploinsufficiency of CSNK2B (loss-of-function mutations leading to reduced CK2β protein via mRNA and protein instability) results in reduced overall CK2 holoenzyme complex formation and reduced kinase activity, identified as the primary pathomechanism of Poirier-Bienvenu syndrome; patient-derived cells with p.Leu39Arg and p.Met132LeufsTer110 variants show mutant mRNA/protein instability. |
In vitro functional assays, western blot, mRNA stability analysis in patient-derived cells, structural and predictive analysis |
Genes |
Medium |
36833176
|
| 2025 |
AAV-PHP.eB-mediated brain-wide CSNK2B gene replacement in Csnk2b haploinsufficient mice restored cortical and hippocampal structure, normalized neuronal numbers and PV-interneuron density, prolonged survival, and ameliorated spontaneous seizures and ASD-like social/cognitive behaviors; EEG signatures (theta/gamma power and inter-areal coherence) were also corrected, indicating re-establishment of excitation/inhibition balance. |
Csnk2b+/– mouse model, neonatal retro-orbital AAV injection, behavioral assays, histology, EEG recording |
bioRxivpreprint |
Medium |
bio_10.1101_2025.10.23.684260
|