We are sorry, but NCBI web applications do not support your browser and may not function properly. More information

Results: 4

1.
Figure 1

Figure 1. From: Biomarkers and Mechanisms of FANCD2 Function.

Hypersensitivity of FANCD2-deficient human fibroblasts to DNA damage. (a) Clonogenic survival of cells with or without wild-type FANCD2 (PD20-wtD2 or PD20, resp.) after treatment with varying concentrations of MMC for one hour. (b) Analogously, clonogenic survival after exposure to hydrogen peroxide (H2O2) for two hours. Data represent logarithmic means +/− standard error based on four independent repeats.

Henning Willers, et al. J Biomed Biotechnol. 2008;2008:821529.
2.
Figure 2

Figure 2. From: Biomarkers and Mechanisms of FANCD2 Function.

Resistance of FANCA-mutant cells with defective FANCD2 function to hydrogen peroxide (H2O2). (a) Representative images illustrating staining for subnuclear FANCD2 foci in isogenic fibroblast pairs, either deficient for FANCD2 (PD20) or FANCA (PD220) and their respective wild-type (wt) complemented counterparts. Foci were visualized three hours after treatment with H2O2 (25 μM for 2 hours). (b) Clonogenic survival of cells with or without wild-type FANCA after treatment with varying concentrations of H2O2. Data represent logarithmic means +/− standard error from 15-repeat experiments.

Henning Willers, et al. J Biomed Biotechnol. 2008;2008:821529.
3.
Figure 4

Figure 4. From: Biomarkers and Mechanisms of FANCD2 Function.

DNA damage and cell survival as a function of FANCD2 status. (a) Representative images of the formation of γH2AX foci in PD20 versus wild-type complemented cells 30 minutes after completion of H2O2 treatment. (b) Quantification of γH2AX foci response. Data represent means with upper standard error based on two independent experiments. (c) G2-type chromosomal aberrations are expressed as breaks per cell as a function of increasing H2O2 concentration in FANCD2-deficient and wild-type complemented PD20 cells. Data represent means with SEM based on at least three repeat experiments. (d) Apoptosis induction by H2O2 (50 μM) in cells with or without wild-type FANCD2 using fluorescence microscopy to assess apoptotic morphology by DAPI staining and flow cytometric analysis for sub-G1 DNA content. Representative experiments based on the apoptotic response at 24 hours are shown (similar results were obtained at 48 hours and with 25 μM H2O2).

Henning Willers, et al. J Biomed Biotechnol. 2008;2008:821529.
4.
Figure 3

Figure 3. From: Biomarkers and Mechanisms of FANCD2 Function.

Normal DNA damage responses in FANCD2-deficient cells treated with hydrogen peroxide (H2O2). (a) Illustration of RAD51 foci formation in PD20 and PD20-wtD2 cells 5 hours after exposure to MMC (0.25 μg/mL for 1 hour) or H2O2 (25 μM for 2 hours). (b) Induction of RAD51 foci formation above background levels by MMC or H2O2. Because equal drug concentrations were used, rather than isoeffective concentrations with regard to cell survival, the extent of foci induction between FANCD-deficient and -complemented cells is not directly comparable. Data represent means with upper standard error based on three independent repeats. (c) DNA synthesis measured by BrdU pulse labeling in cells treated with ionizing radiation (IR, 8 Gy) or H2O2 (25 μM). Data represent means with upper standard error based on two independent experiments. (d) Cell cycle distribution of propidium-iodide cell populations by flow cytometry. A representative experiment is shown. Percentages of cells in the G1, S, and G2 (and M) phases of the cell cycle are indicated.

Henning Willers, et al. J Biomed Biotechnol. 2008;2008:821529.

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Write to the Help Desk