Cell cycle arrest is sufficient for p53-mediated tumor regression
نویسندگان
چکیده
منابع مشابه
Tumor Suppression in the Absence of p53-Mediated Cell-Cycle Arrest, Apoptosis, and Senescence
Cell-cycle arrest, apoptosis, and senescence are widely accepted as the major mechanisms by which p53 inhibits tumor formation. Nevertheless, it remains unclear whether they are the rate-limiting steps in tumor suppression. Here, we have generated mice bearing lysine to arginine mutations at one (p53(K117R)) or three (p53(3KR); K117R+K161R+K162R) of p53 acetylation sites. Although p53(K117R/K11...
متن کاملSUMOylation of hnRNP-K is required for p53-mediated cell-cycle arrest in response to DNA damage.
Heterogeneous ribonucleoprotein-K (hnRNP-K) is normally ubiquitinated by HDM2 for proteasome-mediated degradation. Under DNA-damage conditions, hnRNP-K is transiently stabilized and serves as a transcriptional co-activator of p53 for cell-cycle arrest. However, how the stability and function of hnRNP-K is regulated remained unknown. Here, we demonstrated that UV-induced SUMOylation of hnRNP-K p...
متن کاملp53 is dispensable for UV-induced cell cycle arrest at late G(1) in mammalian cells.
Genotoxic agents, including gamma-rays and UV light, induce transient arrest at different phases of the cell cycle. These arrests are required for efficient repair of DNA lesions, and employ several factors, including the product of the tumor suppressor gene p53 that plays a central role in the cellular response to DNA damage. p53 protein has a major function in the gamma-ray-induced cell cycle...
متن کاملH2AX is required for cell cycle arrest via the p53/p21 pathway.
Phosphorylation of H2AX (gammaH2AX) is an early sign of DNA damage induced by replication stalling. However, the role of H2AX in the repair of this type of DNA damage is still unclear. In this study, we used an inactivated adeno-associated virus (AAV) to induce a stalled replication fork signal and investigate the function of gammaH2AX. The cellular response to AAV provides a unique model to st...
متن کاملRegulation of p53-mediated apoptosis and cell cycle arrest by Steel factor.
Activation of the p53 protein can lead to apoptosis and cell cycle arrest. In contrast, activation of the signalling pathway controlled by the Kit receptor tyrosine kinase prevents apoptosis and promotes cell division of a number of different cell types in vivo. We have investigated the consequences of activating the Kit signalling pathway by its ligand Steel factor on these opposing functions ...
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ژورنال
عنوان ژورنال: Gene Therapy
سال: 2001
ISSN: 0969-7128,1476-5462
DOI: 10.1038/sj.gt.3301592