Figure 1
Schematic structure of TP53 and p53, and numbers of mutations in exons in lymphoid malignancies. (A) TP53 gene structure, p53 functional domains, and posttranslational modifications. Exons are in blue (UTRs) or green (CDS) and are drawn proportionally to their sizes; introns are dark blue and not drawn to scale. Sizes of exons/introns are according to NCBI (reference NC_000017.10 sequence). Domains of p53 include transactivation domain (TAD), proline-rich domain (PRD), DBD, nuclear localization sequence (NLS), oligomerization domain (OD), and basic/repression (BR) of DBD. Both the TAD and OD have a nuclear export signal (NES). Posttranslational modification of p53 can occur by phosphorylation (P), acetylation (A), ubiquitination (U), methylation (M), neddylation (N), or sumoylation (S). (B) Schematic of p53 protein structure. Shown are positions in the p53 primary sequence for 3 loops (L1, L2, L3) involved in DNA binding, 11 β-strands (S1-S10) as components of 2 anti-parallel β-sheets, and 3 α-helices, including 2 in the helix-loop-helix motif. (C) TP53 CDS mutation numbers in lymphoid malignancies. These mutations are not randomly distributed, as indicated by the finding that mutation numbers (shown on right side and illustrated by the length of red bars) in each exon are not proportional to exon sizes (on the left side). Mutation numbers (unique mutation variants and sample/mutation associations) are according to the IARC TP53 database (R15 release, November 2010).

Schematic structure of TP53 and p53, and numbers of mutations in exons in lymphoid malignancies. (A) TP53 gene structure, p53 functional domains, and posttranslational modifications. Exons are in blue (UTRs) or green (CDS) and are drawn proportionally to their sizes; introns are dark blue and not drawn to scale. Sizes of exons/introns are according to NCBI (reference NC_000017.10 sequence). Domains of p53 include transactivation domain (TAD), proline-rich domain (PRD), DBD, nuclear localization sequence (NLS), oligomerization domain (OD), and basic/repression (BR) of DBD. Both the TAD and OD have a nuclear export signal (NES). Posttranslational modification of p53 can occur by phosphorylation (P), acetylation (A), ubiquitination (U), methylation (M), neddylation (N), or sumoylation (S). (B) Schematic of p53 protein structure. Shown are positions in the p53 primary sequence for 3 loops (L1, L2, L3) involved in DNA binding, 11 β-strands (S1-S10) as components of 2 anti-parallel β-sheets, and 3 α-helices, including 2 in the helix-loop-helix motif. (C) TP53 CDS mutation numbers in lymphoid malignancies. These mutations are not randomly distributed, as indicated by the finding that mutation numbers (shown on right side and illustrated by the length of red bars) in each exon are not proportional to exon sizes (on the left side). Mutation numbers (unique mutation variants and sample/mutation associations) are according to the IARC TP53 database (R15 release, November 2010).

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