| Product Name |
Recombinant Mouse Kinase, DNA Activated, Catalytic Polypeptide (PRKDC) Protein |
| Product Overview |
This recombinant mouse Kinase, DNA Activated, Catalytic Polypeptide (PRKDC) protein includes amino acids 3899-4128aa of the target gene is expressed in E.coli.The protein is supplied in lyophilized form and formulated in PBSprior to lyophilization. |
| Target Uniprot Id |
P97313 |
| Recommended Name |
DNA-dependent protein kinase catalytic subunit |
| Gene Name |
Prkdc |
| Synonyms |
HYRC; HYRC1; DNPK1; p350; DNAPK; XRCC7; DNA-PKcs |
| Species |
Mouse |
| Predicted Molecular Mass |
30 kDa |
| Expression System |
E.coli |
| Expression Range |
3899-4128aa |
| Tag |
N-6His |
| Purity |
>90% |
| Formulation |
Lyophilized |
| Buffer |
PBS |
| Storage Condition |
1. Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. 2. Avoid repeated freeze-thaw cycles. 3. Store working aliquots at 4°C for up to one week. 4. In general, protein in liquid form is stable for up to 6 months at -20°C/-80°C. Protein in lyophilized powder form is stable for up to 12 months at -20°C/-80°C. |
| Reconstitution Instruction |
Briefly centrifuged the vial prior to opening to bring the contents to the bottom. Reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL. It is recommended to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. The default final concentration of glycerol is 50%. |
| Applications |
Positive Control; Immunogen; SDS-PAGE; WB |
| Research Area |
Others |
| Target Function |
Serine/threonine-protein kinase that acts as a molecular sensor for DNA damage. Involved in DNA non-homologous end joining (NHEJ) required for double-strand break (DSB) repair and V(D)J recombination. Must be bound to DNA to express its catalytic properties. Promotes processing of hairpin DNA structures in V(D)J recombination by activation of the hairpin endonuclease artemis (DCLRE1C). Recruited by XRCC5 and XRCC6 to DNA ends and is required to (1) protect and align broken ends of DNA, thereby preventing their degradation, (2) and sequester the DSB for repair by NHEJ. Act as a scaffold protein to aid the localization of DNA repair proteins to the site of damage. The assembly of the DNA-PK complex at DNA ends is also required for the NHEJ ligation step. Found at the ends of chromosomes, suggesting a further role in the maintenance of telomeric stability and the prevention of chromosomal end fusion. Also involved in modulation of transcription. As part of the DNA-PK complex, involved in the early steps of ribosome assembly by promoting the processing of precursor rRNA into mature 18S rRNA in the small-subunit processome. Binding to U3 small nucleolar RNA, recruits PRKDC and XRCC5/Ku86 to the small-subunit processome. Recognizes the substrate consensus sequence [ST]-Q. Phosphorylates 'Ser-139' of histone variant H2AX, thereby regulating DNA damage response mechanism. Phosphorylates DCLRE1C, c-Abl/ABL1, histone H1, HSPCA, c-jun/JUN, p53/TP53, PARP1, POU2F1, DHX9, FH, SRF, NHEJ1/XLF, XRCC1, XRCC4, XRCC5, XRCC6, WRN, MYC and RFA2. Can phosphorylate C1D not only in the presence of linear DNA but also in the presence of supercoiled DNA. Ability to phosphorylate p53/TP53 in the presence of supercoiled DNA is dependent on C1D. Contributes to the determination of the circadian period length by antagonizing phosphorylation of CRY1 'Ser-588' and increasing CRY1 protein stability, most likely through an indirect mechanism. Plays a role in the regulation of DNA virus-mediated innate immune response by assembling into the HDP-RNP complex, a complex that serves as a platform for IRF3 phosphorylation and subsequent innate immune response activation through the cGAS-STING pathway. |
| Subcellular Location |
Nucleus. Nucleus, nucleolus. |
| Protein Family |
PI3/PI4-kinase family |
| Associated Diseases |
Defects in Prkdc are the cause of severe combined immune deficiency (SCID) which is characterized by a lack of mature functional lymphocytes and a high susceptibility to lethal opportunistic infections if not chronically treated with antibiotics. The lack of B- and T-cell immunity resembles severe combined immunodeficiency syndrome in human infants. |
