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CSNK2A2 (casein kinase 2 alpha 2)

Written2020-11Nazanin Abazari, Alessandro Beghini
University of Milan, Department of Health Sciences, Milan Italy Nazanin.abazari@studenti.unimi.it; alessandro.beghini@unimi.it

Abstract CSNK2A2 gene, 16q21, has a role in regulating the phosphorylation and circulation of old proteasomes by encoding the catalytic α' subunit of casein kinase 2 (CK2α'). Casein kinase 2 is a serine/threonine protein kinase that phosphorylates acidic proteins. It can regulate Wnt signalling by phosphorylating CTNNB1 and the transcription factor LEF1 and for this reason, it is involved in some cellular key processes such as cell cycle progression, inhibition of apoptosis, DNA damage repair, differentiation and transcription but also viral infection. CSNK2A2 is a cancer-related gene and its upregulation has been detected is many cancers such as glioblastoma multiforme, colorectal cancer, breast cancer and ovarian cancer, and also in some diseases such as diabetes, theileriasis in cattle and distal muscular dystrophy with anterior tibial onset in mice are associated with CSNK2A2.

Keywords Kinase; Serine/threonine-protein kinase; CSNK2A2; CK2A2; CSNK2A1; CK2alpha

(Note : for Links provided by Atlas : click)

Identity

Alias (NCBI)CK2A2
CSNK2A1
CK2alpha
HGNC (Hugo) CSNK2A2
HGNC Alias symbCSNK2A1
CK2alpha'
HGNC Alias namecasein kinase 2 alpha'
HGNC Previous name"casein kinase 2, alpha prime polypeptide"
LocusID (NCBI) 1459
Atlas_Id 40171
Location 16q21  [Link to chromosome band 16q21]
Location_base_pair Starts at 58157908 and ends at 58198106 bp from pter ( according to GRCh38/hg38-Dec_2013)  [Mapping CSNK2A2.png]
Local_order chr16 (hg38), Starts at 58157907 and ends at 58198106 bp from pter. (ACCORDING TO CON 17-AUG-2020)
 
  Figure 1. CSNK2A2 gene
Fusion genes
(updated 2017)
Data from Atlas, Mitelman, Cosmic Fusion, Fusion Cancer, TCGA fusion databases with official HUGO symbols (see references in chromosomal bands)

DNA/RNA

Description DNA size: 40200 bp, DNA linear, on reverse strand. This gene has 6 transcripts (splice variants), 412 orthologues, 2 paralogues and is a member of 1 Ensembl protein family.
Transcription CSNK2A2-201 ENST00000262506.8: mRNA 1887 bp, protein 350 aa
CSNK2A2-202 ENST00000562367.1: mRNA 687 bp, No protein
CSNK2A2-203 ENST00000563307.1: mRNA 4978 bp, protein 152 aa
CSNK2A2-204 ENST00000565188.1: mRNA 547 bp, protein 135 aa
CSNK2A2-205 ENST00000566813.5: mRNA 1569 bp, No protein
CSNK2A2-206 ENST00000567730.6: mRNA 947 bp, protein 230 aa (www.ensembl.org).
Pseudogene A related transcribed pseudogene is found on chromosome 11.

Protein

 
  Figure 2. CSNK2A2 (ck2) protein
Description CK2 (casein kinase 2) is an evolutionarily protected protein kinase, and the deletion of both of its catalytic subunits is lethal. (Padmanabha et al., 1990).
The crystal structure of a fully active form (Tetramer) of human CK2 consisting of two C-terminally truncated (Alpha) catalytic and two regulatory (Beta) subunits (Protein Data Bank code: 1JWH). This protein is composed of 350 amino acids, with Molecular mass of 41213 Da. For two α subunits, α being 42 kDa and α' being 38 kDa, and two β subunits, each weighing in at 28 kDa. The β subunits form homodimers which are building blocks to generate heterotetramers with the catalytic subunits (α or α') in which these two catalytic subunits in the holoenzyme make no contacts with each other (Niefind, Guerra et al. 2001). CK2 proteins can function as monomeric kinases or within a tetrameric complex of two CK2 kinase units and two units of the regulatory protein CK2b. ((Ortega, Seidner et al. 2014).
Quaternary structure is generally characterized by tight regulation. The enzyme acts independently of classical activating second messengers. (Ackermann, Neidhart et al. 2005). Unlike most other proteins, CK2 shows the rare ability 'dual-co-substrate specificity' to use either ATP or GTP as phosphoryl donor. (Niefind et al., 1999).
CSNK2A2 encodes alpha prime polypeptide (the catalytic subunit of the protein kinase enzyme). The α subunits do not require the β regulatory subunits to function, this allows dimers to form of the catalytic domains independent of β subunit transcription. Catalytic subunit of kinase complex phosphorylates a large number of substrates containing acidic residues C-terminal to the phosphorylated serine or threonine such as casein (Pinna 2002). In mouse transgenic models CK2α is an oncogene and CK2α overexpression in mammary gland and lymphoid compartment leads to tumor formation (Seldin 1995).
CSNK2A2 protein also has interactions with other proteins such as CSNK2B, CSNK2A1, ENSG00000263020, JUN , TP53, SUPT16H, SSRP1, DVL3, DVL1, NFKBIA. https://www.sinobiological.com/resource/ck2-alpha-csnk2a1/proteins
 
  Figure 3. Sequence alignment
Expression In human, CSNK2A2 has a broad expression in testis (RPKM 55.0) and skin (RPKM 19.3) but also it is expressed in 24 other tissues including bone marrow, whole blood, lymph node, thymus, cerebellum, brain, retina, spinal cord, heart, smooth muscle, skeletal muscle, small intestine, colon, adipocyte, kidney, liver, lung, pancreas, thyroid, salivary gland, adrenal gland, ovary, uterus, placenta, cervix and prostate (Ortega, Seidner et al. 2014). https://www.genecards.org/cgi-bin/carddisp.pl?gene=CSNK2A2#expression.
A significant increase in expression of eight Wnt signaling pathway proteins including CSNK2A2, was detected in glioblastoma multiforme (GBM) (Shevchenko, Arnotskaya et al. 2020).
Experimental studies suggest that irregular expression of the alpha CK2 subunit transmits a oncogenic potential in the cells such that in cooperation with certain oncogenes it causes a profound increase in tumor phenotype. (Tawfic, Yu et al. 2001).
In addition, increased CSNK2A2 expression has been observed in breast cancer tissue and breast cancer cell lines, colon cancer progression as well as villous colon adenomas (Romieu-Mourez, Landesman-Bollag et al. 2001, Nibbe, Markowitz et al. 2009, Nguyen, Albers et al. 2010, Wang, Chang et al. 2016). Moreover, data on transcript expression of the specified gene (CK2) in cancer versus normal tissue revealed widespread upregulation in the expression of CK2 genes in primary tumor tissues (Ortega, Seidner et al. 2014).
 
  Figure4. CSNK2A2 (ck2) mRNA Expression in different tumor types GTXportal.org/home/gene/.
Localisation CSNK2A2 is localized in the nucleus and cytosol. Nuclear matrix and chromatin described to be the key sites for signaling of the CK2 activity in relation to cell growth (Tawfic, Yu et al. 2001).
 
  Figure 5. CSNK2A2 (ck2) in wnt signaling
Function CSNK2A2 is responsible for phosphorylation of substrates containing acidic residues in various pathways within a cell; ATP or GTP can be used as phosphate source. Indeed, it can regulate numerous cellular processes, such as cell cycle progression, apoptosis, and transcription, as well as viral infection.
During mitosis CK2s anti-apoptotic function is in the continuation of the cell cycle; from G1 to S phase and G2 to M phase checkpoints, it functions as a component of the TP53-dependent spindle assembly checkpoint (SAC) that maintains cyclin-B- CDK1 activity and G2 arrest in response to spindle damage.
Comparison the induced expression of catalytically inactive CK2a in human osteosarcoma U2-OS cells suggested that CK2α' may have unique functions associated with the control of proliferation or viability.
CSNK2A2 is also required for TP53-mediated apoptosis, phosphorylating 'Ser-392' of TP53 following UV irradiation.
CSNK2A2 also regulates transcription by direct phosphorylation of RNA polymerases I, II, III and IV. Also phosphorylates and regulates numerous transcription factors including NF-kappa-B, STAT1, CREB1, IRF1, IRF2, ATF1, SRF, MAX, JUN, FOS, MYC and MYB. Phosphorylates HSP90AA1 (Hsp90) and its co-chaperones FKBP4 and CDC37, which is essential for chaperone function.
It acts as an ectokinase that phosphorylates several extracellular proteins. During viral infection, phosphorylates various proteins involved in the viral life cycles of EBV, HSV, HBV, HCV, HIV, CMV and HPV (Keller, Zeng et al. 2001, Sayed, Pelech et al. 2001, Shin, Lee et al. 2005).
The Wnt pathway connection:
CSNK2A2 acts as a multi-site regulator of the Wnt pathway, and it is well known for phosphorylating CTNNB1 (β-catenin ) and the transcription factor LEF1.
Wnt signaling is initiated by binding of the secreted Wnt ligand to the members of the Frizzled receptor family. The level of β-catenin in the cytosol, is a key element in the Wnt pathway which triggers the activation of Wnt responsive genes. In the absence of Wnt stimulation, β-catenin is degraded by the proteasome (which depends upon β-catenin phosphorylation in a multi-protein complex by a hierarchical mechanism involving both CSNK1A1 (CK1) and GSK3). This phosphorylation is crucial for binding of β-catenin to the F-box protein βTrCP, which imparts specficity on the ubiquitination apparatus.
Wnt signaling inhibits GSK3 and prevents the ubiquitination and degradation of β-catenin, which leads to the accumulation of β-catenin in the cytosol and the activation of Wnt responsive genes, some of which are proto-oncogenes.
It is hypothesized that CK2 has dual role in the Wnt signaling pathway. First it can directly phosphorylate β-catenin and prevents its degradation by counteracting the effect of GSK3 phosphorylation within the negative regulatory complex (Son et al., 2000). Inhibition of CK2 decreases β-catenin level and blocks proliferation of Wnt-transfected cells. Suggesting that β-catenin phosphorylated by CK2 escapes ubiquitination and degradation, leading to an increased level of β-catenin available to activate Wnt-responsive genes.
On the other hand, CK2, by phosphorylating CDC34 (the E2 ubiquitin-conjugating enzyme UBC3), promotes its binding to the proteasome receptor β-TrCP, ultimately assisting the degradation of β-catenin (Semplici et al., 2002).
The apoptosis pathway connection:
Under survival conditions, CK2 phosphorylates proteins such as ARC and BID. When ARC is phosphorylated, it is targeted to mitochondria, where it inhibits CASP8 (caspase 8). Bid is resistant to cleavage by caspase 8, when it is phosphorylated by CK2. Under apoptotic conditions, CK2 phosphorylation sites on proteins such as BID and ARC are not phosphorylated, indeed ARC is not targeted to mitochondria and does not inhibit caspase 8. In the absence of phosphorylation, Bid is susceptible to cleavage by caspase 8.
The subsequent translocation of BID to the mitochondria is followed by release of cytochrome C that leads to the amplification of caspase activation (proteins, including MAX and HS1, become susceptible to caspase-mediated cleavage when they are not phosphorylated by CK2) (Litchfield 2003).
CSNK2A2 can also negatively regulate apoptosis by phosphorylating the caspases ( CASP9 and CASP2) and the apoptotic regulator NOL3. This phosphorylation, protects CASP9 from cleavage and activation by CASP8, so can inhibits the CASP2 dimerization and CASP8 activation.
 
  Figure 6. CSNK2A2 (ck2) and apoptosis
Homology The CSNK2A2 gene is conserved in chimpanzee, Rhesus monkey, dog, cow, mouse, rat, chicken, zebrafish, S.cerevisiae, K.lactis, E.gossypii, A.thaliana, and rice.

Mutations

Note First human condition associated with germline mutations in any of the CK2 subunits has been described by Volkan Okur (Volkan Okur, 2016 Jul) with a clinical phenotype of neurodevelopmental disabilities and dysmorphic features. Patients from five independent families with overlapping neurodevelopmental disorders and dysmorphic features were found to have likely damaging de novo splice site or missense variants in highly conserved regions of CSNK2A1. They found one splice site variant (c.824 + 2T>C) and four missense variants (p.R47Q, p.Y50S, p.D175G, p.K198R) in this gene.
 
  Figure 7. 3D structure of human CSNK2A2 and mutation sites
 
  Figure 8. Domains of CSNK2A1 and locations of de novo variants.
 
  Figure 9. Predicted pathogenicity of novel de novo CSNK2A1 variants
Somatic Somatic mutations in CSNK2A1 have been implicated in various cancers by regulating downstream cancer-associated genes such as JAK/STAT, NF-kB, PI3K/AKT (Zheng et al. 2013).

Implicated in

  
Entity Diabetes
Note Researchers investigated the relationship of relative leukocyte telomere length (RTL) with cardiometabolic risk. Genome-wide association study (GWAS) and meta-analysis identified two variants (rs7196068 and rs74019828) in CSNK2A2 which are associated with leukocyte telomere length in a Punjabi Sikh diabetic cohort.
CSNK2A2 is affiliated with the members of the shelterin complex involved in chromosome-end protection, telomere regulation, and maintenance. Interestingly, the telomeric repeat binding factor 1 ( TERF1) serves as a substrate for CSNK2A2, which phosphorylates and initiates its binding to telomeres. Partial knock-down of CSNK2A2 resulted in removal of TERF1 from telomeres and degradation of TERF1.
CSNK2A2 also influences Wnt signaling via beta-catenin phosphorylation and the PI3-K signaling pathway via the phosphorylation of Akt (Saxena, Bjonnes et al. 2014).
  
  
Entity Epithelial ovarian cancer (EOC)
Note Ovarian cancer is the leading cause of death for gynecologic cancers, ranking fifth overall for cancer-related death among women. The function of protein kinase CK2α (CK2α) in EOC is still unknown. Study on the EOC cell lines (like A2780, HO8910, COV644, OVCAR3, SKOV3) and the primary normal ovarian surface epithelial (NOSE) cells revealed that CK2α protein expression was increased in A2780, HO8910, OVCAR3, and SKOV3 ovarian cancer cell lines compared to the NOSE cells. In addition, CK2α knockdown by specific siRNAs, inhibited migration, and invasion ability of OVCAR3 and SKOV3 cells. Study of Zebiao Ma suggests that, CK2α may play a role in tumor aggressive behavior of EOC and could be used as a marker for predicting prognosis of EOC patient, plus high CK2α expression might predict poor patient survival (Ma, Wang et al. 2017)
  
  
Entity Triple negative breast cancer (TNBC)
Note Increased CK2 protein expression and activity is observed in a broad range of cancers including breast cancer. Aggressive breast cancers like triple-negative breast cancer (TNBC) refers to any breast cancer that does not express the genes for estrogen receptors ESR1 and ESR2), progesterone receptor (PGR) and epidermal growth factor receptor 2 ( ERBB2 (HER2/neu)). Lacking HER2 overexpression, makes it more difficult to be treated, since most hormone therapies target one of these three receptors, therefore this feature of TNBC have improved mortality. Casein kinase 2 (CK2) is a survival protein kinase that suppresses cancer cell death. RNA expression levels analysis revealed strong CDK11 and CK2 mRNA as well as protein expression in most human breast cancer cells. Down-regulation of CDK11 and/or CK2 in breast cancer cells caused significant loss of cell viability and clonal survival, suggesting that CDK11 and CK2 expression are individually essential for breast cancer cell survival including TNBC and they serve as promising new targets for therapeutic development in breast cancer (Kren, Unger et al. 2015).
  
  
Entity Colorectal cancer (CRC)
Note It has been identified that several proteins (CSNK2A2, PLK1, and IGFBP3) are associated with the progression of colorectal cancer (CRC). CSNK2A2 in CRC, suppresses apoptosis by desensitizing cells to TRAIL in a caspase-dependent manner but independent of NF-kβ. It has also been shown to promote survival of colon cancer cells by increasing the expression of survivin via the canonical transcription pathway hyperactive in CRC ( LEF1 (lymphoid enhancer binding factor) )(Nibbe, Markowitz et al. 2009).
  
  
Entity Glioblastoma multiforme (GBM)
Note In a study, researchers compared the expression levels of signaling pathway proteins in CD133(+) CSCs and CD133 (-) differentiated glioblastoma cells (DGCs). This revealed a significant increase in expression of eight Wnt signalling pathway proteins ( APC, CSNK1E, CSNK1A1, CSNK2A2, CSNK2B, CTNNB1, DVL1, CHTF18 (RUVBL)) in cancer stem cells (CSCs) of Glioblastoma multiforme (GBM). Two catalytic subunits (CSNK2A2 and CSNK2B) has been identified with higher expression levels (3.01 - 3.04 fold) in CSCs as compared with DGCs (Shevchenko, Arnotskaya et al. 2020).
  

Bibliography

The catalytic subunit alpha' gene of human protein kinase CK2 (CSNK2A2): genomic organization, promoter identification and determination of Ets1 as a key regulator
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Mol Cell Biochem 2005 Jun;274(1-2):91-101.
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A DNA damage-induced p53 serine 392 kinase complex contains CK2, hSpt16, and SSRP1
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Mol Cell 2001 Feb;7(2):283-92.
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Preclinical evaluation of cyclin dependent kinase 11 and casein kinase 2 survival kinases as RNA interference targets for triple negative breast cancer therapy
Kren BT, Unger GM, Abedin MJ, Vogel RI, Henzler CM, Ahmed K, Trembley JH
Breast Cancer Res 2015;17:19.
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Protein kinase CK2: structure, regulation and role in cellular decisions of life and death
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Increased expression of protein kinase CK2α correlates with poor patient prognosis in epithelial ovarian cancer
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Differentiation of tubular and villous adenomas based on Wnt pathway-related gene expression profiles
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Discovery and scoring of protein interaction subnetworks discriminative of late stage human colon cancer
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Crystal structure of human protein kinase CK2: insights into basic properties of the CK2 holoenzyme
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Mining CK2 in cancer
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Roles of IKK kinases and protein kinase CK2 in activation of nuclear factor-kappaB in breast cancer
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Genome-wide association study identifies variants in casein kinase II (CSNK2A2) to be associated with leukocyte telomere length in a Punjabi Sikh diabetic cohort
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Protein kinase CK2 is involved in G2 arrest and apoptosis following spindle damage in epithelial cells
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Citation

This paper should be referenced as such :
Abazari N, Beghini A
CSNK2A2 (casein kinase 2 alpha 2);
Atlas Genet Cytogenet Oncol Haematol. in press


Other Leukemias implicated (Data extracted from papers in the Atlas) [ 1 ]
  t(5;16)(q11;q21) MAP3K1/CSNK2A2


External links

Nomenclature
HGNC (Hugo)CSNK2A2   2459
Cards
AtlasCSNK2A2ID40171ch16q21
Entrez_Gene (NCBI)CSNK2A2    casein kinase 2 alpha 2
AliasesCK2A2; CK2alpha'; CSNK2A1
GeneCards (Weizmann)CSNK2A2
Ensembl hg19 (Hinxton)ENSG00000070770 [Gene_View]
Ensembl hg38 (Hinxton)ENSG00000070770 [Gene_View]  ENSG00000070770 [Sequence]  chr16:58157908-58198106 [Contig_View]  CSNK2A2 [Vega]
ICGC DataPortalENSG00000070770
TCGA cBioPortalCSNK2A2
AceView (NCBI)CSNK2A2
Genatlas (Paris)CSNK2A2
SOURCE (Princeton)CSNK2A2
Genetics Home Reference (NIH)CSNK2A2
Genomic and cartography
GoldenPath hg38 (UCSC)CSNK2A2  -     chr16:58157908-58198106 -  16q21   [Description]    (hg38-Dec_2013)
GoldenPath hg19 (UCSC)CSNK2A2  -     16q21   [Description]    (hg19-Feb_2009)
GoldenPathCSNK2A2 - 16q21 [CytoView hg19]  CSNK2A2 - 16q21 [CytoView hg38]
ImmunoBaseENSG00000070770
genome Data Viewer NCBICSNK2A2 [Mapview hg19]  
OMIM115442   
Gene and transcription
Genbank (Entrez)AI150700 AI332952 AK090752 AK125922 BC008812
RefSeq transcript (Entrez)NM_001896
RefSeq genomic (Entrez)
Consensus coding sequences : CCDS (NCBI)CSNK2A2
Alternative Splicing GalleryENSG00000070770
Gene ExpressionCSNK2A2 [ NCBI-GEO ]   CSNK2A2 [ EBI - ARRAY_EXPRESS ]   CSNK2A2 [ SEEK ]   CSNK2A2 [ MEM ]
Gene Expression Viewer (FireBrowse)CSNK2A2 [ Firebrowse - Broad ]
GenevisibleExpression of CSNK2A2 in : [tissues]  [cell-lines]  [cancer]  [perturbations]  
BioGPS (Tissue expression)1459
GTEX Portal (Tissue expression)CSNK2A2
Human Protein AtlasENSG00000070770-CSNK2A2 [pathology]   [cell]   [tissue]
Protein : pattern, domain, 3D structure
UniProt/SwissProtP19784   [function]  [subcellular_location]  [family_and_domains]  [pathology_and_biotech]  [ptm_processing]  [expression]  [interaction]
NextProtP19784  [Sequence]  [Exons]  [Medical]  [Publications]
With graphics : InterProP19784
Splice isoforms : SwissVarP19784
PhosPhoSitePlusP19784
Domaine pattern : Prosite (Expaxy)PROTEIN_KINASE_ATP (PS00107)    PROTEIN_KINASE_DOM (PS50011)    PROTEIN_KINASE_ST (PS00108)   
Domains : Interpro (EBI)Kinase-like_dom_sf    Prot_kinase_dom    Protein_kinase_ATP_BS    Ser/Thr_kinase_AS   
Domain families : Pfam (Sanger)Pkinase (PF00069)   
Domain families : Pfam (NCBI)pfam00069   
Domain families : Smart (EMBL)S_TKc (SM00220)  
Conserved Domain (NCBI)CSNK2A2
Blocks (Seattle)CSNK2A2
PDB (RSDB)3E3B    3OFM    3U87    5M4U    5M56    5OOI    5Y9M    5YF9    5YWM    6HMB    6HMC    6HMD    6HMQ    6QY9   
PDB Europe3E3B    3OFM    3U87    5M4U    5M56    5OOI    5Y9M    5YF9    5YWM    6HMB    6HMC    6HMD    6HMQ    6QY9   
PDB (PDBSum)3E3B    3OFM    3U87    5M4U    5M56    5OOI    5Y9M    5YF9    5YWM    6HMB    6HMC    6HMD    6HMQ    6QY9   
PDB (IMB)3E3B    3OFM    3U87    5M4U    5M56    5OOI    5Y9M    5YF9    5YWM    6HMB    6HMC    6HMD    6HMQ    6QY9   
Structural Biology KnowledgeBase3E3B    3OFM    3U87    5M4U    5M56    5OOI    5Y9M    5YF9    5YWM    6HMB    6HMC    6HMD    6HMQ    6QY9   
SCOP (Structural Classification of Proteins)3E3B    3OFM    3U87    5M4U    5M56    5OOI    5Y9M    5YF9    5YWM    6HMB    6HMC    6HMD    6HMQ    6QY9   
CATH (Classification of proteins structures)3E3B    3OFM    3U87    5M4U    5M56    5OOI    5Y9M    5YF9    5YWM    6HMB    6HMC    6HMD    6HMQ    6QY9   
SuperfamilyP19784
Human Protein Atlas [tissue]ENSG00000070770-CSNK2A2 [tissue]
Peptide AtlasP19784
HPRD00279
IPIIPI00020602   
Protein Interaction databases
DIP (DOE-UCLA)P19784
IntAct (EBI)P19784
BioGRIDCSNK2A2
STRING (EMBL)CSNK2A2
ZODIACCSNK2A2
Ontologies - Pathways
QuickGOP19784
Ontology : AmiGOchromatin  acrosomal vesicle  protein serine/threonine kinase activity  protein serine/threonine kinase activity  protein binding  ATP binding  nucleus  nucleus  nucleus  nucleoplasm  cytosol  cytosol  plasma membrane  protein kinase CK2 complex  protein folding  phosphatidylcholine biosynthetic process  apoptotic process  cell cycle  spermatogenesis  Wnt signaling pathway  macroautophagy  peptidyl-serine phosphorylation  peptidyl-serine phosphorylation  peptidyl-threonine phosphorylation  cerebral cortex development  PcG protein complex  PcG protein complex  protein N-terminus binding  regulation of cell cycle  liver regeneration  regulation of signal transduction by p53 class mediator  regulation of autophagy of mitochondrion  positive regulation of protein targeting to mitochondrion  regulation of chromosome separation  regulation of chromosome separation  negative regulation of ubiquitin-dependent protein catabolic process  negative regulation of apoptotic signaling pathway  
Ontology : EGO-EBIchromatin  acrosomal vesicle  protein serine/threonine kinase activity  protein serine/threonine kinase activity  protein binding  ATP binding  nucleus  nucleus  nucleus  nucleoplasm  cytosol  cytosol  plasma membrane  protein kinase CK2 complex  protein folding  phosphatidylcholine biosynthetic process  apoptotic process  cell cycle  spermatogenesis  Wnt signaling pathway  macroautophagy  peptidyl-serine phosphorylation  peptidyl-serine phosphorylation  peptidyl-threonine phosphorylation  cerebral cortex development  PcG protein complex  PcG protein complex  protein N-terminus binding  regulation of cell cycle  liver regeneration  regulation of signal transduction by p53 class mediator  regulation of autophagy of mitochondrion  positive regulation of protein targeting to mitochondrion  regulation of chromosome separation  regulation of chromosome separation  negative regulation of ubiquitin-dependent protein catabolic process  negative regulation of apoptotic signaling pathway  
Pathways : KEGGRibosome biogenesis in eukaryotes    NF-kappa B signaling pathway    Wnt signaling pathway    Adherens junction    Tight junction    Measles    Herpes simplex infection    Epstein-Barr virus infection   
REACTOMEP19784 [protein]
REACTOME PathwaysR-HSA-8948751 [pathway]   
NDEx NetworkCSNK2A2
Atlas of Cancer Signalling NetworkCSNK2A2
Wikipedia pathwaysCSNK2A2
Orthology - Evolution
OrthoDB1459
GeneTree (enSembl)ENSG00000070770
Phylogenetic Trees/Animal Genes : TreeFamCSNK2A2
HOGENOMP19784
Homologs : HomoloGeneCSNK2A2
Homology/Alignments : Family Browser (UCSC)CSNK2A2
Gene fusions - Rearrangements
Fusion : MitelmanMAP3K1/CSNK2A2 [5q11.2/16q21]  
Fusion : Fusion_HubCFAP20--CSNK2A2    CSNK2A2--C16ORF80    CSNK2A2--PPM1K    FBN2--CSNK2A2    MLKL--CSNK2A2    RAB7A--CSNK2A2    RP11-459F6.1--CSNK2A2    RPL10--CSNK2A2    SRGAP2--CSNK2A2    TADA3--CSNK2A2    USP10--CSNK2A2   
Fusion : QuiverCSNK2A2
Polymorphisms : SNP and Copy number variants
NCBI Variation ViewerCSNK2A2 [hg38]
dbVarCSNK2A2
ClinVarCSNK2A2
MonarchCSNK2A2
1000_GenomesCSNK2A2 
Exome Variant ServerCSNK2A2
GNOMAD BrowserENSG00000070770
Varsome BrowserCSNK2A2
Genomic Variants (DGV)CSNK2A2 [DGVbeta]
DECIPHERCSNK2A2 [patients]   [syndromes]   [variants]   [genes]  
CONAN: Copy Number AnalysisCSNK2A2 
Mutations
ICGC Data PortalCSNK2A2 
TCGA Data PortalCSNK2A2 
Broad Tumor PortalCSNK2A2
OASIS PortalCSNK2A2 [ Somatic mutations - Copy number]
Somatic Mutations in Cancer : COSMICCSNK2A2  [overview]  [genome browser]  [tissue]  [distribution]  
Somatic Mutations in Cancer : COSMIC3DCSNK2A2
Mutations and Diseases : HGMDCSNK2A2
LOVD (Leiden Open Variation Database)Whole genome datasets
LOVD (Leiden Open Variation Database)LOVD 3.0 shared installation
BioMutasearch CSNK2A2
DgiDB (Drug Gene Interaction Database)CSNK2A2
DoCM (Curated mutations)CSNK2A2 (select the gene name)
CIViC (Clinical Interpretations of Variants in Cancer)CSNK2A2 (select a term)
intoGenCSNK2A2
NCG6 (London) select CSNK2A2
Cancer3DCSNK2A2(select the gene name)
Impact of mutations[PolyPhen2] [Provean] [Buck Institute : MutDB] [Mutation Assessor] [Mutanalyser]
Diseases
OMIM115442   
Orphanet
DisGeNETCSNK2A2
MedgenCSNK2A2
Genetic Testing Registry CSNK2A2
NextProtP19784 [Medical]
GENETestsCSNK2A2
Target ValidationCSNK2A2
Huge Navigator CSNK2A2 [HugePedia]
ClinGenCSNK2A2
Clinical trials, drugs, therapy
MyCancerGenomeCSNK2A2
Protein Interactions : CTD
Pharm GKB GenePA26959
PharosP19784
Clinical trialCSNK2A2
Miscellaneous
canSAR (ICR)CSNK2A2 (select the gene name)
HarmonizomeCSNK2A2
DataMed IndexCSNK2A2
Probes
Litterature
PubMed260 Pubmed reference(s) in Entrez
GeneRIFsGene References Into Functions (Entrez)
EVEXCSNK2A2
REVIEW articlesautomatic search in PubMed
Last year publicationsautomatic search in PubMed

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