Transient activation of p53 in G2 phase is sufficient to induce senescence.
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Activation of DNA Damage Response Induced by the Kaposi's Sarcoma-Associated Herpes VirusCell-based screen for altered nuclear phenotypes reveals senescence progression in polyploid cells after Aurora kinase B inhibition.Hypersensitivity to DNA damage in antephase as a safeguard for genome stability.Replication stress in Mammalian cells and its consequences for mitosisSenescence from G2 arrest, revisitedWIP1 phosphatase as pharmacological target in cancer therapy.Bystander communication and cell cycle decisions after DNA damagePhosphorylation of Tip60 by p38α regulates p53-mediated PUMA induction and apoptosis in response to DNA damageOncogenic Herpesvirus Utilizes Stress-Induced Cell Cycle Checkpoints for Efficient Lytic ReplicationMitotic Stress Is an Integral Part of the Oncogene-Induced Senescence Program that Promotes Multinucleation and Cell Cycle ArrestFanconi anemia cells with unrepaired DNA damage activate components of the checkpoint recovery process.SCF(Fbxo22)-KDM4A targets methylated p53 for degradation and regulates senescence.Ageing and the pathogenesis of osteoarthritis.Mitotic catastrophe and cell cycle arrest are alternative cell death pathways executed by bortezomib in rituximab resistant B-cell lymphoma cellsKey points of basic theories and clinical practice in rAd-p53 ( Gendicine ™) gene therapy for solid malignant tumors.FUCCI sensors: powerful new tools for analysis of cell proliferation.The emerging role of senescent cells in tissue homeostasis and pathophysiology.ATM/Wip1 activities at chromatin control Plk1 re-activation to determine G2 checkpoint duration.New origin firing is inhibited by APC/CCdh1 activation in S-phase after severe replication stressTousled-like kinase 2 regulates recovery from a DNA damage-induced G2 arrest.MicroRNA Regulation of Oxidative Stress-Induced Cellular Senescence53BP1 Integrates DNA Repair and p53-Dependent Cell Fate Decisions via Distinct Mechanisms.Inhibition of WIP1 phosphatase sensitizes breast cancer cells to genotoxic stress and to MDM2 antagonist nutlin-3.Residual Cdk1/2 activity after DNA damage promotes senescence.Enter the nucleus to exit the cycle.The Chromatin Remodeling Component Arid1a Is a Suppressor of Spontaneous Mammary Tumors in Mice.Cdk2 strengthens the intra-S checkpoint and counteracts cell cycle exit induced by DNA damage.How the cell cycle enforces senescence.Inhibition of coiled coil domain containing protein 69 enhances platinum-induced apoptosis in ovarian cancer cells.Orchestration of DNA Damage Checkpoint Dynamics across the Human Cell Cycle.Metabolic perturbation of epigenome by inhibiting S-adenosylhomocysteine hydrolase elicits senescence through DNA damage response in hepatoma cells.MicroRNA-16 mediates the regulation of a senescence-apoptosis switch in cutaneous T-cell and other non-Hodgkin lymphomas.The live cell DNA stain SiR-Hoechst induces DNA damage responses and impairs cell cycle progression.Ionizing Radiation-Induced Cellular Senescence in Normal, Non-transformed Cells and the Involved DNA Damage Response: A Mini Review.Photoactivation of MDM2 Inhibitors: Controlling Protein-Protein Interaction with LightCardiomyocyte gene programs encoding morphological and functional signatures in cardiac hypertrophy and failureFoxM1 repression during human aging leads to mitotic decline and aneuploidy-driven full senescencePersistent repair intermediates induce senescenceA limited number of double-strand DNA breaks is sufficient to delay cell cycle progressionAgeing, Cellular Senescence and Neurodegenerative Disease
P2860
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P2860
Transient activation of p53 in G2 phase is sufficient to induce senescence.
description
2014 nî lūn-bûn
@nan
2014年の論文
@ja
2014年学术文章
@wuu
2014年学术文章
@zh-cn
2014年学术文章
@zh-hans
2014年学术文章
@zh-my
2014年学术文章
@zh-sg
2014年學術文章
@yue
2014年學術文章
@zh
2014年學術文章
@zh-hant
name
Transient activation of p53 in G2 phase is sufficient to induce senescence.
@en
Transient activation of p53 in G2 phase is sufficient to induce senescence.
@nl
type
label
Transient activation of p53 in G2 phase is sufficient to induce senescence.
@en
Transient activation of p53 in G2 phase is sufficient to induce senescence.
@nl
prefLabel
Transient activation of p53 in G2 phase is sufficient to induce senescence.
@en
Transient activation of p53 in G2 phase is sufficient to induce senescence.
@nl
P50
P1433
P1476
Transient activation of p53 in G2 phase is sufficient to induce senescence
@en
P2093
Femke M Feringa
P356
10.1016/J.MOLCEL.2014.05.007
P577
2014-06-05T00:00:00Z