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. Author manuscript; available in PMC: 2013 Dec 1.

Published in final edited form as: DNA Repair (Amst). 2012 Oct 17;11(12):942–950. doi: 10.1016/j.dnarep.2012.09.003

Fig. 1 — XP-B and XP-B/CS fibroblasts are defective in accumulation of CAK component MAT1 at DNA damage sites in vivo. Normal human fibroblasts (NHF) (A), XP-B fibroblasts XP33BR (B), XP-B/CS fibroblasts XPCS1BA (C) and XP183MA (D) were grown on coverslips, locally irradiated with 100 J/m² UV through a 5 μm-isopore polycarbonate filter, fixed immediately (0 h) or cultured for 0.5, 3, or 24 h before fixing in 2% paraformaldehyde. The TFIIH component p62 and CAK component MAT1 were visualized by immunofluorescence double labeling using specific antibodies. Nuclei shown in blue are from counterstaining with DAPI. Arrows indicate immunofluorescent foci due to accumulation of THIIH proteins at localized damage sites.

Fig. 1 — XP-B and XP-B/CS fibroblasts are defective in accumulation of CAK component MAT1 at DNA damage sites in vivo. Normal human fibroblasts (NHF) (A), XP-B fibroblasts XP33BR (B), XP-B/CS fibroblasts XPCS1BA (C) and XP183MA (D) were grown on coverslips, locally irradiated with 100 J/m² UV through a 5 μm-isopore polycarbonate filter, fixed immediately (0 h) or cultured for 0.5, 3, or 24 h before fixing in 2% paraformaldehyde. The TFIIH component p62 and CAK component MAT1 were visualized by immunofluorescence double labeling using specific antibodies. Nuclei shown in blue are from counterstaining with DAPI. Arrows indicate immunofluorescent foci due to accumulation of THIIH proteins at localized damage sites.