Dcaf11, also known as Ddb1- and Cul4-associated factor 11, is an E3 ligase substrate adaptor [2]. It is involved in multiple biological processes, such as telomere elongation, targeted protein degradation, and cell cycle regulation. It plays a crucial role in maintaining chromosome stability and cellular protein homeostasis [1,2]. Genetic models, especially KO/CKO mouse models, can be valuable in studying its functions.

Deletion of Dcaf11 in embryos and embryonic stem cells leads to reduced telomere sister-chromatid exchange (T-SCE) and impaired telomere lengthening. Dcaf11-deficient mice exhibit gradual telomere erosion over successive generations, and hematopoietic stem cell (HSC) activity is compromised, indicating its importance in telomere elongation in early embryos [1]. In human osteosarcoma cells, knocking down components of the CRL4BDCAF11 complex, including DCAF11, attenuates the ubiquitination level of p21Cip1, inhibits cell proliferation, leads to cell cycle arrest at S phase, and decreases colony formation rate, suggesting its role in cell cycle progression [3].

In conclusion, Dcaf11 is essential for telomere elongation in early embryos and for regulating cell cycle progression in osteosarcoma cells. Studies using KO/CKO mouse models have provided valuable insights into its role in maintaining chromosome stability and cell cycle-related disease conditions like osteosarcoma [1,3].