Prkdc-KO Mouse

Prkdc, encoding the DNA-dependent protein kinase catalytic subunit (DNA-PKcs), is crucial for nonhomologous end-joining DNA repair, a pathway vital for maintaining genomic stability [3]. It is involved in multiple biological processes and has significant implications for various diseases [3,5]. Genetic models, such as gene knockout (KO) and conditional knockout (CKO) mouse models, are valuable for studying Prkdc's functions.

In osteosarcoma, loss-of-function experiments showed that the loss of Prkdc significantly increased sensitivity to doxorubicin (DOX), as Prkdc recruited and bound GDE2 to enhance GNAS stability, which activated AKT phosphorylation and conferred DOX resistance [1].

In gastric cancer, hsa_circ_0136666 upregulated Prkdc expression by sponging miR-375-3p, regulating immune checkpoint proteins, and driving PD-L1 phosphorylation and immune escape [2].

In skin wound healing, knockdown of circ_PRKDC promoted keratinocyte migration during wound healing through the miR-31/FBN1 axis [4].

In conclusion, Prkdc plays essential roles in DNA repair, and its dysregulation is associated with various diseases. KO/CKO mouse models have revealed its role in cancer chemoresistance, tumor immune escape, and skin wound healing, providing potential therapeutic targets for these disease areas.