Figure 4.
Figure 4. CLL patients with FBXW7 mutations have increased NICD levels. (A) Cleaved NOTCH1 (NICD) and (B) c-MYC protein levels were determined in primary CLL cells from patients with and without FBXW7 mutations. Different NICD band sizes of patients 7 and 8 might be due to degradation products of NICD or due to different posttranslational modifications. (C) Translation in primary CLL patient cells was inhibited by 10 µg/mL cycloheximide (CHX) for the indicated periods of time. NICD and c-MYC protein levels were analyzed via western blotting. Stable c-MYC levels in patient 5 might be observable due to MYC lesions or dysregulation of other proteins responsible for c-MYC degradation. Loading control for patients 2, 5, 6, and 9 is β-actin, for patients 3, 7, and 8 the loading control is α-tubulin. NOTCH1 ΔCT mut, NOTCH1 deletion of a CT dinucleotide (P2514fs); pat, patient.

CLL patients with FBXW7 mutations have increased NICD levels. (A) Cleaved NOTCH1 (NICD) and (B) c-MYC protein levels were determined in primary CLL cells from patients with and without FBXW7 mutations. Different NICD band sizes of patients 7 and 8 might be due to degradation products of NICD or due to different posttranslational modifications. (C) Translation in primary CLL patient cells was inhibited by 10 µg/mL cycloheximide (CHX) for the indicated periods of time. NICD and c-MYC protein levels were analyzed via western blotting. Stable c-MYC levels in patient 5 might be observable due to MYC lesions or dysregulation of other proteins responsible for c-MYC degradation. Loading control for patients 2, 5, 6, and 9 is β-actin, for patients 3, 7, and 8 the loading control is α-tubulin. NOTCH1 ΔCT mut, NOTCH1 deletion of a CT dinucleotide (P2514fs); pat, patient.

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