Ataxin-7-like protein 3 (ATXN7L3)

Ataxin-7-like protein 3 (ATXN7L3) is a non-enzymatic adaptor subunit of the SAGA (Spt–Ada–GCN5 acetyltransferase) complex, which is essential for transcriptional activation via chromatin remodeling and specifically through the removal of monoubiquitin from histone H2B by the deubiquitination module (DUBm) partnering with USP22 and ENY2[1][4]. ATXN7L3 facilitates nuclear receptor coactivator activity and is critical for proper gene expression, counteracting heterochromatin silencing and supporting transcription by RNA polymerase II[1][4]. Dysregulation or mutation (including gene fusion with UBTF) can result in altered chromatin dynamics and is implicated in various pathologies, notably certain cancers such as hepatocellular carcinoma and acute lymphoblastic leukemia[1][2]. ATXN7L3 localizes in the nucleus and contains a conserved SCA7 zinc-finger domain vital for its function within the SAGA complex[1][3][4]. It has no known direct pharmacological antagonists or drugs, but its role in gene regulation and disease suggests potential value as a therapeutic target or a biomarker, especially in cancer diagnostics and stratification[2][4].

Other names

Ataxin-7-like protein 3ATXN7L3DKFZp761G2113SAGA-associated factor 11 homologSGF11ataxin-7-like protein 3