Active Recombinant Human CSNK2A2 protein(Met1-Arg350), His&GST-tagged

• Cat.No.: CSNK2A2-969H
• Product Overview: Recombinant Human CSNK2A2 (NP_001887.1) (Met 1-Arg 350) was expressed in Insect Cells, fused with the N-terminal polyhistidine-tagged GST tag at the N-terminus.

Specification

• Species: Human
• Source: Insect Cells
• Tag: GST&His
• Protein Length: Met1-Arg350
• Form: Supplied as sterile 50mM Tris, 500mM NaCl, 0.5mM PMSF, 0.5mM TCEP, 10% gly, pH 8.5.
• Bio-activity: The specific activity was determined to be 30 nmol/min/mg using casein as substrate.
• Molecular Mass: The recombinant human CSNK2A2/GST chimera consists of 587 amino acids and has a calculated molecular mass of 69 kDa. It migrates as an approximately 60 kDa band in SDS-PAGE under reducing conditions.
• Endotoxin: < 1.0 EU per μg of the protein as determined by the LAL method.
• Purity: > 92 % as determined by SDS-PAGE
• Storage: Samples are stable for up to twelve months from date of receipt at -20°C to -80°C. Store it under sterile conditions at -20°C to -80°C. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
• Concentration: Please refer to the hard copy of CoA.

Gene Information

• Gene Name: CSNK2A2 casein kinase 2, alpha prime polypeptide [ Homo sapiens ]
• Official Symbol: CSNK2A2
• Synonyms: CSNK2A2; casein kinase 2, alpha prime polypeptide; casein kinase II subunit alpha; CSNK2A1; CK II alpha; CK2A2; FLJ43934
• Gene ID: 1459
• mRNA Refseq: NM_001896
• Protein Refseq: NP_001887
• MIM: 115442
• UniProt ID: P19784

Case Study

Case 1: Wu D, et al. Hepatobiliary Pancreat Dis Int. 2023

Liver cancer's high mortality is partly because cancer stems cells resist chemo, and CK2α seems to play a part. It's overactive in tumors, boosting growth and resistance to treatment, altering stem cell markers, and helping cells invade. But when CK2α is reduced, these effects are reversed, pointing to its role via the Hedgehog pathway.

Fig1. The expression levels of CK2α protein were examined using Western blotting.

Fig2. Isolation of CD133(-) and CD133(+) cell populations from HepG2 cells overexpressing CK2α.

Case 2: Ruggeri E, et al. Front Immunol. 2024

In classical Hodgkin lymphoma, tumor cells thrive thanks to the NF-κB, JAK/STAT, and PI3K/Akt pathways. A key player here is CK2, a kinase with two parts, α and β, and usually, both subunits go overboard in cancers. In cHL, CK2α is up, while CK2β is down—often tagged for destruction in cells. Blocking CK2 with CX-4945/silmitasertib stops important pathways, leading to cell death and lowers PD-L1, enhancing the effects of cancer drugs like MMAE.

Fig1. Protein expression levels of CK2 alpha (α) and beta (β) subunits in HL cell lines.

Fig2. Expression of CK2 subunits according to the grading level.

Application

The recombinant CSNK2A2 protein is like the Swiss Army knife of research tools. It's integral to so many cellular processes—think cell cycles, DNA repair, you name it. Researchers can't get enough of it because it holds clues to how cells manage to do all their incredible stuff, like how they grow or fix themselves. If you're in the lab researching cancer or how cells develop, CSNK2A2 is often your go-to buddy. In the realm of drug discovery, CSNK2A2 is turning heads. Researchers are eager to see if it can be a prime target for new cancer treatments. The idea is that by curbing CK2's activity, we might be able to stop cancer cells in their tracks. It's like zeroing in on a loose cog in a machine—fix that, and you just might keep the whole contraption from breaking down.

Fig1. Simplistic representation of influence of CK2 signalling in nuclear matrix. (P R Blanquet, 2000)