Arsenic-induced PML targeting onto nuclear bodies: implications for the treatment of acute promyelocytic leukemia
about
PML nuclear bodiesCommon properties of nuclear body protein SP100 and TIF1alpha chromatin factor: role of SUMO modificationSp100 interacts with ETS-1 and stimulates its transcriptional activityHuman SIR2 deacetylates p53 and antagonizes PML/p53-induced cellular senescence.Arsenic-induced SUMO-dependent recruitment of RNF4 into PML nuclear bodiesLeukemia-associated retinoic acid receptor alpha fusion partners, PML and PLZF, heterodimerize and colocalize to nuclear bodiesZIP kinase triggers apoptosis from nuclear PML oncogenic domainsRNF4 is a poly-SUMO-specific E3 ubiquitin ligase required for arsenic-induced PML degradationTRIM family proteins: retroviral restriction and antiviral defenceViral immediate-early proteins abrogate the modification by SUMO-1 of PML and Sp100 proteins, correlating with nuclear body disruptionConjugation with the ubiquitin-related modifier SUMO-1 regulates the partitioning of PML within the nucleus.Arsenic trioxide is a potent inhibitor of the interaction of SMRT corepressor with Its transcription factor partners, including the PML-retinoic acid receptor alpha oncoprotein found in human acute promyelocytic leukemiaCaspase cleavage of MST1 promotes nuclear translocation and chromatin condensationThe human and African green monkey TRIM5alpha genes encode Ref1 and Lv1 retroviral restriction factor activitiesFrom an old remedy to a magic bullet: molecular mechanisms underlying the therapeutic effects of arsenic in fighting leukemiaThe cell biology of disease: Acute promyelocytic leukemia, arsenic, and PML bodiesArsenic Trioxide Inhibits Hepatitis C Virus RNA Replication through Modulation of the Glutathione Redox System and Oxidative StressTargeting of leukemia-initiating cells in acute promyelocytic leukemiaPML protein isoforms and the RBCC/TRIM motifPML interaction with p53 and its role in apoptosis and replicative senescencePIC-1/SUMO-1-modified PML-retinoic acid receptor alpha mediates arsenic trioxide-induced apoptosis in acute promyelocytic leukemiaRole of promyelocytic leukemia (PML) sumolation in nuclear body formation, 11S proteasome recruitment, and As2O3-induced PML or PML/retinoic acid receptor alpha degradationArsenic trioxide induces apoptosis of HPV16 DNA-immortalized human cervical epithelial cells and selectively inhibits viral gene expressionArsenic trioxide induces apoptosis in neuroblastoma cell lines through the activation of caspase 3 in vitroArsenic-induced apoptosis in malignant cells in vitroApoptosis and growth inhibition in malignant lymphocytes after treatment with arsenic trioxide at clinically achievable concentrationsTRIM5 alpha cytoplasmic bodies are highly dynamic structures.The tumor suppressor cybL, a component of the respiratory chain, mediates apoptosis inductionPathologic, cytogenetic and molecular assessment of acute promyelocytic leukemia patients treated with arsenic trioxide (As2O3).Retinoic acid, but not arsenic trioxide, degrades the PLZF/RARalpha fusion protein, without inducing terminal differentiation or apoptosis, in a RA-therapy resistant t(11;17)(q23;q21) APL patient.Retinoic acid and arsenic synergize to eradicate leukemic cells in a mouse model of acute promyelocytic leukemiaArsenic trioxide triggers a regulated form of caspase-independent necrotic cell death via the mitochondrial death pathway.Arsenic trioxide controls the fate of the PML-RARalpha oncoprotein by directly binding PML.Maintenance therapy with all-trans retinoic acid and arsenic trioxide improves relapse-free survival in adults with low- to intermediate-risk acute promyelocytic leukemia who have achieved complete remission after consolidation therapy.The pathogenesis of acute promyelocytic leukaemia: evaluation of the role of molecular diagnosis and monitoring in the management of the disease.The disruption of ND10 during herpes simplex virus infection correlates with the Vmw110- and proteasome-dependent loss of several PML isoformsModulation of p53, c-fos, RARE, cyclin A, and cyclin D1 expression in human leukemia (HL-60) cells exposed to arsenic trioxideInteractions of herpes simplex virus type 1 with ND10 and recruitment of PML to replication compartments.PTEN is a negative regulator of mitotic checkpoint complex during the cell cycleArsenic trioxide therapy for relapsed acute promyelocytic leukemia: an useful salvage therapy.
P2860
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P2860
Arsenic-induced PML targeting onto nuclear bodies: implications for the treatment of acute promyelocytic leukemia
description
1997 nî lūn-bûn
@nan
1997 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
1997 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
1997年の論文
@ja
1997年論文
@yue
1997年論文
@zh-hant
1997年論文
@zh-hk
1997年論文
@zh-mo
1997年論文
@zh-tw
1997年论文
@wuu
name
Arsenic-induced PML targeting ...... f acute promyelocytic leukemia
@ast
Arsenic-induced PML targeting ...... f acute promyelocytic leukemia
@en
Arsenic-induced PML targeting ...... f acute promyelocytic leukemia
@nl
type
label
Arsenic-induced PML targeting ...... f acute promyelocytic leukemia
@ast
Arsenic-induced PML targeting ...... f acute promyelocytic leukemia
@en
Arsenic-induced PML targeting ...... f acute promyelocytic leukemia
@nl
prefLabel
Arsenic-induced PML targeting ...... f acute promyelocytic leukemia
@ast
Arsenic-induced PML targeting ...... f acute promyelocytic leukemia
@en
Arsenic-induced PML targeting ...... f acute promyelocytic leukemia
@nl
P2093
P2860
P356
P1476
Arsenic-induced PML targeting ...... f acute promyelocytic leukemia
@en
P2093
M K Chelbi-Alix
P2860
P304
P356
10.1073/PNAS.94.8.3978
P407
P577
1997-04-15T00:00:00Z