Abstract
Vitamin D and its receptor, VDR, together and independently, have been associated with DNA repair, though the mechanism by which they act is unclear. Upon ultraviolet irradiation through 3 mm pores in otherwise opaque filters to create focal spots of DNA damage, epidermal keratinocytes from both VDR-null mice and human keratinocytes depleted of VDR with siRNA exhibited slower removal of 6-4 photoproducts than normal control cells over 90 minutes. Co-staining with antibodies to XPC, the initial UV-induced DNA damage recognition sensor, revealed that XPC rapidly accumulated at DNA damage foci and gradually faded over 90 minutes as nucleotide excision repair proceeded in control human keratinocytes.
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
