NDLI: Transformer2 proteins protect breast cancer cells from accumulating replication stress by ensuring productive splicing of checkpoint kinase 1

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Transformer2 proteins protect breast cancer cells from accumulating replication stress by ensuring productive splicing of checkpoint kinase 1

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Transformer2 proteins protect breast cancer cells from accumulating replication stress by ensuring productive splicing of checkpoint kinase 1

Content Provider	Springer Nature Link
Author	Best, Andrew James, Katherine Hysenaj, Gerald Tyson Capper, Alison Elliott, David J.
Copyright Year	2015
Abstract	Increased expression levels of the RNA splicing regulator Transformer2β (abbreviated Tra2β) have been reported in several types of cancer. Recent work has revealed an intimate cross-regulation between Tra2β and the highly similar Tra2α protein in human breast cancer cells, though these two proteins are encoded by separate genes created by a gene duplication that occurred over 500 million years ago. This cross-regulation involves splicing control of a special class of exons, called poison exons. Down-regulation of Tra2β reduces splicing inclusion of a poison exon in the mRNA encoding Tra2α, thereby up-regulating Tra2α protein expression. This buffers any splicing changes that might be caused by individual depletion of Tra2β alone. Discovery of this cross-regulation pathway, and its by-pass by joint depletion of both human Tra2 proteins, revealed Tra2 proteins are essential for breast cancer cell viability, and led to the identification of important targets for splicing control. These exons include a critical exon within the checkpoint kinase 1 (CHK1) gene that plays a crucial function in the protection of cancer cells from replication stress. Breast cancer cells depleted for Tra2 proteins have reduced CHK1 protein levels and accumulate DNA damage. These data suggest Tra2 proteins and/or their splicing targets as possible cancer drug targets.
Starting Page	186
Ending Page	195
Page Count	10
File Format	PDF
ISSN	20950179
Journal	Frontiers of Chemical Engineering in China
Volume Number	10
Issue Number	2
e-ISSN	20950187
Language	English
Publisher	Higher Education Press
Publisher Date	2015-11-05
Publisher Institution	Chinese Universities
Publisher Place	Beijing
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	RNA splicing gene expression breast cancer DNA damage CHK1 Industrial Chemistry/Chemical Engineering Nanotechnology
Content Type	Text
Resource Type	Article
Subject	Chemical Engineering

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Targeting the Checkpoint to Kill Cancer Cells

Functions, Regulation, and Therapeutic Implications of the ATR Checkpoint Pathway

DNA damage checkpoint maintenance through sustained Chk1 activity

Phosphorylation of Minichromosome Maintenance 3 (MCM3) by Checkpoint Kinase 1 (Chk1) Negatively Regulates DNA Replication and Checkpoint Activation

Ubiquitination of the DNA-damage checkpoint kinase CHK1 by TRAF4 is required for CHK1 activation

The Interaction between Checkpoint Kinase 1 (Chk1) and the Minichromosome Maintenance (MCM) Complex Is Required for DNA Damage-induced Chk1 Phosphorylation

Chromosome 11q loss and MYCN amplification demonstrate synthetic lethality with checkpoint kinase 1 inhibition in neuroblastoma

Distinct but Concerted Roles of ATR, DNA-PK, and Chk1 in Countering Replication Stress during S Phase

New Insights into Checkpoint Kinase 1 (Chk1) in the DNA Damage Response (DDR) Signaling Network: Rationale for Employing Chk1 Inhibitors in Cancer Therapeutics

Transformer2 proteins protect breast cancer cells from accumulating replication stress by ensuring productive splicing of checkpoint kinase 1

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Transformer2 proteins protect breast cancer cells from accumulating replication stress by ensuring productive splicing of checkpoint kinase 1