Genomic instability is a hallmark of cancer cells which results in excessive DNA damage. To counteract this, cells have evolved a tightly regulated DNA damage response (DDR) to rapidly sense DNA damage and promote its repair whilst halting cell cycle progression. The DDR functions predominantly within the context of chromatin and requires the action of chromatin-binding proteins to coordinate the appropriate response. TRIM24, TRIM28, TRIM33 and TRIM66 make up the transcriptional intermediary factor 1 (TIF1) family of chromatin-binding proteins, a subfamily of the large tripartite motif (TRIM) family of E3 ligases. All four TIF1 proteins are aberrantly expressed across numerous cancer types, and increasing evidence suggests that TIF1 family members can function to maintain genome stability by mediating chromatin-based responses to DNA damage. This review provides an overview of the TIF1 family in cancer, focusing on their roles in DNA repair, chromatin regulation and cell cycle regulation.
|Number of pages||18|
|Publication status||Published - Aug 2020|
- DNA damage
- Genome stability
ASJC Scopus subject areas
- Cancer Research
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Investigating the role of TRIM33 in the DNA damage response in multiple MyelomaAuthor: McAvera, R., Jul 2022
Supervisor: Crawford, L. (Supervisor) & Mills, K. (Supervisor)
Student thesis: Doctoral Thesis › Doctor of Philosophy