TIF1 Proteins in Genome Stability and Cancer

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 with...

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Main Authors: Roisin M. McAvera, Lisa J. Crawford
Format: Article
Language:English
Published: MDPI AG 2020-07-01
Series:Cancers
Subjects:
Online Access:https://www.mdpi.com/2072-6694/12/8/2094
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author Roisin M. McAvera
Lisa J. Crawford
author_facet Roisin M. McAvera
Lisa J. Crawford
author_sort Roisin M. McAvera
collection DOAJ
description 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.
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spelling doaj.art-42df7cc8999e4a36a08fc7b8eef40eab2023-11-20T08:14:29ZengMDPI AGCancers2072-66942020-07-01128209410.3390/cancers12082094TIF1 Proteins in Genome Stability and CancerRoisin M. McAvera0Lisa J. Crawford1Patrick G Johnston Centre for Cancer Research, Queen’s University Belfast, Belfast BT9 7AE, UKPatrick G Johnston Centre for Cancer Research, Queen’s University Belfast, Belfast BT9 7AE, UKGenomic 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.https://www.mdpi.com/2072-6694/12/8/2094TRIM24TRIM28TRIM33TRIM66genome stabilityDNA damage
spellingShingle Roisin M. McAvera
Lisa J. Crawford
TIF1 Proteins in Genome Stability and Cancer
Cancers
TRIM24
TRIM28
TRIM33
TRIM66
genome stability
DNA damage
title TIF1 Proteins in Genome Stability and Cancer
title_full TIF1 Proteins in Genome Stability and Cancer
title_fullStr TIF1 Proteins in Genome Stability and Cancer
title_full_unstemmed TIF1 Proteins in Genome Stability and Cancer
title_short TIF1 Proteins in Genome Stability and Cancer
title_sort tif1 proteins in genome stability and cancer
topic TRIM24
TRIM28
TRIM33
TRIM66
genome stability
DNA damage
url https://www.mdpi.com/2072-6694/12/8/2094
work_keys_str_mv AT roisinmmcavera tif1proteinsingenomestabilityandcancer
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