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. Author manuscript; available in PMC: 2020 Sep 1.
Published in final edited form as: Best Pract Res Clin Haematol. 2019 Jun 6;32(3):196–206. doi: 10.1016/j.beha.2019.06.003

Figure 1. Somatic mutation frequencies of Homo sapiens STAT3 in hematological malignancies and comparison of STAT3 and STAT5B amino acid sequences.

Figure 1.

STAT3 mutations specific to hematopoietic and lymphoid tissue were downloaded from COSMIC and cBio portal (STAT3 accession # NM_139276) and shown as lollipop plots. Domains are N-terminal, coiled-coil, DNA binding, linker, Src homology 2 (SH2), and transactivation (TA) (A-D). STAT3 mutation frequency is listed for (A) LGL leukemia (B) ATL, MDS, and NK/T lymphoma, and (C) all other hematological malignancies. Green, black, red, and pink circles indicate missense, truncation, in-frame, or other mutations, respectively. (D) STAT3 (alpha isoform) and STAT5B Homo sapiens amino acid sequences were retrieved from the NCBI Protein Database (accession # NP_644805 for STAT3, NP_036580 for STAT5B). The sequences were aligned using Clustal Omega, The C-terminal sequence including the SH2 and TA domains are shown. Asterisks indicate a fully-conserved amino acid at a position, while colons and periods indicate conserved and semi-conserved substitutions, respectively. STAT3 and STAT5B somatic mutations are annotated in red and blue, respectively. In two cases (Y640F and N647I) the STAT3 mutation creates the innate STAT5B amino acid.