TRIM25 promotes Capicua degradation independently of ERK in the absence of ATXN1L.

ABSTRACT:

Background

Aberrations in Capicua (CIC) have recently been implicated as a negative prognostic factor in a multitude of cancer types through the derepression of targets downstream of the mitogen-activated protein kinase (MAPK) signaling cascade, such as oncogenic E26 transformation-specific (ETS) transcription factors. The Ataxin-family protein ATXN1L has previously been reported to interact with CIC in both developmental and disease contexts to facilitate the repression of CIC target genes and promote the post-translational stability of CIC. However, little is known about the mechanisms at the base of ATXN1L-mediated CIC post-translational stability.

Results

Functional in vitro studies utilizing ATXN1L^KO human cell lines revealed that loss of ATXN1L leads to the

SUBMITTER: Wong D 

PROVIDER: S-EPMC7594423 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature