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Blood, Vol. 112, Issue 5, 1683-1686, September 1, 2008
Defective homing is associated with altered Cdc42 activity in cells from patients with Fanconi anemia group A
Blood Zhang et al.
112: 1683
Supplemental materials for: Zhang et al
Files in this Data Supplement:
- Figure S1. Decreased Cdc42 activity in FA-C and FA-G cells (JPG, 43 KB)
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(A) Levels of the active, GTP-bound Cdc42 (top panels) in lymphoblasts, derived from FA-C (HSC536), FA-G (RA1329) patients, or two normal donors (Normal 1, JY; Normal 2, HSC93), were determined by the GST-PAK1 pulldown assay followed by Western blotting using an antibody against Cdc42. The relative levels of active Cdc42 are indicated below each pulldown blot. The levels of total Cdc42 (middle panels) and β-actin (bottom panels) are shown as loading controls. (B) Levels of the active, GTP-bound Rac1 in lymphoblasts described in (A), as determined by the GST-PAK1 pulldown assay followed by Western blotting using an antibody against Rac1. β-actin blots are shown as loading controls.
- Figure S2. Defective migration of FA-C and FA-G cells (JPG, 31.6 KB)
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2 × 105 lymphoblast cells derived from FA-C (HSC536), FA-G (RA1329) patients, or two normal donors (Normal 1, JY; Normal 2, HSC93) were loaded to the upper chamber of transwell and allowed to migrate for 5 hrs at 37°C. Cells migrating to the lower chamber, which contains SDF-1α, were quantified. Data represent the percentage of the input. Difference between FA-C and normal donor 1 or between FA-G and normal donor 2 is significant (p < 0.01).
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