Ataxin-7 and Non-stop coordinate SCAR protein levels, subcellular localization, and actin cytoskeleton organization

Abstract

SummarySAGA subunits Ataxin-7 and Non-stop regulate stability and subcellular localization of WRC subunit SCAR. Loss of Ataxin-7 increases, while loss of Non-stop decreases, SCAR protein levels and F-actin network assembly. AbstractAtaxin-7 (Atxn7), a subunit of the SAGA transcriptional coactivator complex, is subject to polyglutamine expansion at the amino terminus, causing spinocerebellar ataxia type 7 (SCA7), a progressive retinal and neurodegenerative disease. Within SAGA, the Atxn7 amino terminus anchors the Non-stop deubiquitinase to the complex. To understand the consequences of

Hepatocellular carcinoma reduces ATXN7L3 to evade estrogen-dependent growth suppression

“…Overexpression of USP22 is associated with increased tumor growth, metastasis, and risk of death from cancer [8] . Recently, ATXN7L3, ENY2, and USP22 were found to be capable of leaving SAGA to meet substrates at a distance [9] . While away from SAGA, ENY2 and ATXN7L3 can swap USP22 for either of deubiquitinases USP27x or USP51 [10] .…”