TADA3 (transcriptional adaptor 3) functions as a conserved transcriptional coactivator and core component of histone acetyltransferase complexes, including the PCAF and SAGA complexes 1. As a component of these complexes, TADA3 participates in histone acetylation and transcriptional regulation 2. TADA3 serves as an important cofactor for p53-dependent transcriptional activation and is essential for p53 activity following DNA damage 2. The protein also regulates granzyme B-mediated apoptosis through modulation of Bid processing via PACS2 3. Dysregulation of TADA3 is associated with multiple cancer types. TADA3 expression is significantly elevated in non-small cell lung cancer (NSCLC) specimens and correlates with poor prognosis 1. TADA3 silencing in NSCLC cells suppressed proliferation, migration, and invasion, while increasing epithelial markers and reducing mesenchymal markers, indicating regulation of epithelial-mesenchymal transition 1. TADA3 knockdown delayed G1/S phase progression and inhibited tumor xenograft growth in vivo 1. Additionally, TADA3 was identified as a hub protein in protein-protein interaction networks associated with hepatocellular carcinoma progression 4. In neurological contexts, TADA3 interacts with DCLK3 kinase in striatal neurons and may contribute to transcriptional regulation and chr3 remodeling relevant to neurodegeneration 5. TADA3 deletion has been implicated in 3p deletion syndrome pathology 6.