ABL1 (v-abl Abelson murine leukemia viral oncogene homolog 1)

9q34.12

1130-1143 amino acids; ABL1 is composed from N-term to C-term of a CAP, a SRC homology 3 (SH3), SH2 and SH1 tyrosine kinase domains, a conserved PXXP motifs to mediate protein-protein interactions, three nuclear localization signal (NLS) motifs, a DNA-binding domain, a globular (G).actin-binding domain, one nuclear export signal (NES), and a conserved filamentous actin-binding domain. Regulates endocytosis, epithelial-to.mesenchymal transition, cell polarity, adhesion, migration and invasion; in response to cellular stress, including DNA damage, ABL1 induces growth arrest and/or apoptosis (review in Greuber et al., 2013).

Apart from the well known role of ABL1 in leukemias, ABL1 has been found overexpressed in a small percentage of breast carcinomas, lung squamous cell carcinomas, and uterine corpus carcinomas.

ZMIZ1 (zinc finger MIZ-type containing 1)

10q22.3

1067 amino acids (aa). ZMIZ1 is composed from N-term to C-term of a proline-rich region (aa 363-555 (334-555 according to Swiss-Prot)), a nuclear localization signal sequence (aa 691-713), a Miz domain (aa 738-790 (Zn finger 727-804 according to Swiss-Prot)), and a proline-rich region (transcriptional activation domain) (aa 824-1067 ((867-1002 according to Swiss-Prot)). The central region between aa 556 and 790 is the primary binding region for AR (Sharma et al., 2003). Sequence specific DNA binding protein. Transcriptional coactivator related to members of the proteatggactin inhibitor of activated STAT (PIAS) family. Co-activator of AR (androgen receptor). Increases ligand-dependent transcriptional activity of AR, SMAD3, and TP53. ZMIZ1 is able to enhance the sumoylation of AR. ZMIZ1 cooperates with NOTCH1 to regulate the C-MYC pathway. ZMIZ1 is overexpressed in a subset of T-ALL (Rakowski et al., 2013).