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Hzf and hCAS/CSE1L: making the right choice in p53-mediated tumour suppression.

Katherine E Ewings, +1 more
- 01 Oct 2007 - 
- Vol. 17, Iss: 10, pp 829-831
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This article is published in Cell Research.The article was published on 2007-10-01 and is currently open access. It has received 7 citations till now.

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Journal ArticleDOI

A Homolog of the Cell Apoptosis Susceptibility Gene Involved in Ovary Development of Chinese Shrimp Fenneropenaeus chinensis

TL;DR: The cell apoptosis susceptibility (CAS) gene is a homolog of the yeast chromosome segregation (CSE1) gene, which functions in cell proliferation and apoptosis, which suggested that FcCAS might function as a nuclear protein.
Journal ArticleDOI

Role of Rad51 and DNA repair in cancer: A molecular perspective.

TL;DR: An overview of the main DNA repair pathways, with special focus on the role played by homologous repair and the RAD51 recombinase protein in the cellular DNA damage response, and a survey of the most promising therapeutic strategies aimed at targeting RAD51 in experimental oncology.
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Effect of combined treatment with progesterone and tamoxifen on the growth and apoptosis of human ovarian cancer cells.

TL;DR: Results indicate that progesterone caused apoptosis and tamoxifen induced G1 arrest in ovarian cancer cells, indicating a synergistic effect on anti-cancer activity.
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Expression of CAS/CSE1L, the Cellular Apoptosis Susceptibility Protein, Correlates With Neoplastic Progression in Barrett's Esophagus.

TL;DR: Findings show changes in CAS/CSE1L during BE progression, which may represent a potential marker for dysplasia/carcinoma and indicate its expression in BE neoplasia should be addressed.
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Cellular apoptosis susceptibility protein (CAS) suppresses the proliferation of breast cancer cells by upregulated cyp24a1.

TL;DR: Observations clarified the previous conflicting results on the cell fates of the breast cells regulated by CAS and provide new insight into the role of CAS in the development of breast cancer.
References
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TIGAR, a p53-Inducible Regulator of Glycolysis and Apoptosis

TL;DR: expression of TIGAR may modulate the apoptotic response to p53, allowing survival in the face of mild or transient stress signals that may be reversed or repaired, and the decrease of intracellular ROS levels in response to TIGar may also play a role in the ability of p53 to protect from the accumulation of genomic damage.
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DRAM, a p53-Induced Modulator of Autophagy, Is Critical for Apoptosis

TL;DR: DRAM (damage-regulated autophagy modulator), a p53 target gene encoding a lysosomal protein that induces macroautophagy, is described as an effector of p53-mediated death and its relationship to p53 function and damage-induced programmed cell death is highlighted.
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ASPP proteins specifically stimulate the apoptotic function of p53.

TL;DR: The expression of ASPP is frequently downregulated in human breast carcinomas expressing wild-type p53 but not mutant p53, therefore, ASPP regulate the tumor suppression function of p53 in vivo.
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Genome-wide localization of the nuclear transport machinery couples transcriptional status and nuclear organization.

TL;DR: It is shown that transcriptional activation of the GAL genes results in their association with nuclear pore proteins, relocation to the nuclear periphery, and loss of RanGEF association, which indicates that the organization of the genome is coupled via transcriptional state to thenuclear transport machinery.
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iASPP oncoprotein is a key inhibitor of p53 conserved from worm to human

TL;DR: iASPP is an evolutionarily conserved inhibitor of p53; inhibition of iASPP by RNA-mediated interference or antisense RNA in C. elegans or human cells, respectively, induces p53-dependent apoptosis and could provide an important new strategy for treating tumors expressing wild-type p53.