JNK activation is a mediator of arsenic trioxide-induced apoptosis in acute promyelocytic leukemia cells.
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Regulation of arsenic trioxide-induced cellular responses by Mnk1 and Mnk2Arsenic trioxide overcomes rapamycin-induced feedback activation of AKT and ERK signaling to enhance the anti-tumor effects in breast cancerA review of arsenic trioxide and acute promyelocytic leukemiaThe novel arsenical Darinaparsin circumvents BRG1-dependent, HO-1-mediated cytoprotection in leukemic cellsExit from arsenite-induced mitotic arrest is p53 dependentBIM-mediated AKT phosphorylation is a key modulator of arsenic trioxide-induced apoptosis in cisplatin-sensitive and -resistant ovarian cancer cellsArsenic trioxide exerts antimyeloma effects by inhibiting activity in the cytoplasmic substrates of histone deacetylase 6Arsenic trioxide induces apoptosis in human platelets via C-Jun NH2-terminal kinase activationGlutathione protects cells against arsenite-induced toxicityEthanol Induces Platelet Apoptosis.Arsenic trioxide cooperates with all trans retinoic acid to enhance mitogen-activated protein kinase activation and differentiation in PML-RARalpha negative human myeloblastic leukemia cells.BIMEL is a key effector molecule in oxidative stress-mediated apoptosis in acute myeloid leukemia cells when combined with arsenic trioxide and buthionine sulfoximineArsenic trioxide-dependent activation of thousand-and-one amino acid kinase 2 and transforming growth factor-beta-activated kinase 1.Arsenic trioxide inhibits nuclear receptor function via SEK1/JNK-mediated RXRalpha phosphorylation.Autophagy is a critical mechanism for the induction of the antileukemic effects of arsenic trioxide.Near infrared imaging of EGFR of oral squamous cell carcinoma in mice administered arsenic trioxideCell cycle arrest and apoptotic cell death in cultured human gastric carcinoma cells mediated by arsenic trioxide.Phase 1 trial and pharmacokinetic study of arsenic trioxide in children and adolescents with refractory or relapsed acute leukemia, including acute promyelocytic leukemia or lymphoma.Sensitivity of leukemic T-cell lines to arsenic trioxide cytotoxicity is dependent on the induction of phosphatase B220/CD45R expression at the cell surface.Epoxyeicosatrienoic acids attenuate reactive oxygen species level, mitochondrial dysfunction, caspase activation, and apoptosis in carcinoma cells treated with arsenic trioxide.Treatment of acute promyelocytic leukemia with single-agent arsenic trioxide.Arsenic-induced pancreatitis.Autophagic degradation of the BCR-ABL oncoprotein and generation of antileukemic responses by arsenic trioxideThe emerging role of arsenic trioxide as an immunomodulatory agent in the management of multiple myeloma.Arsenic trioxide inhibits the proliferation of myeloma cell line through notch signaling pathway.Alkenyl group is responsible for the disruption of microtubule network formation in human colon cancer cell line HT-29 cellsBiological responses to arsenic compoundsDirect binding of arsenic trioxide to AMPK and generation of inhibitory effects on acute myeloid leukemia precursors.Assessment of the involvement of oxidative stress and Mitogen-Activated Protein Kinase signaling pathways in the cytotoxic effects of arsenic trioxide and its combination with sulindac or its metabolites: sulindac sulfide and sulindac sulfone on humArsenic trioxide enhances the cytotoxic effect of thalidomide in a KG-1a human acute mylogenous leukemia cell lineArsenite causes down-regulation of Akt and c-Fos, cell cycle dysfunction and apoptosis in glutathione-deficient cells.A novel arsenical has antitumor activity toward As2O3-resistant and MRP1/ABCC1-overexpressing cell lines.Arsenic degrades PML or PML-RARalpha through a SUMO-triggered RNF4/ubiquitin-mediated pathway.Anion exchanger 2 mediates the action of arsenic trioxide.Arsenic trioxide concentration determines the fate of Ewing's sarcoma family tumors and neuroblastoma cells in vitro.ATR, PML, and CHK2 play a role in arsenic trioxide-induced apoptosis.Activation of the mitogen- and stress-activated kinase 1 by arsenic trioxide.Downregulation of mitogen-activated protein kinase 1 of Leishmania donovani field isolates is associated with antimony resistance.Biological effects of Atra and Arsenic Trioxide on short term cultures of non-M3 leukemic blasts.MAPK1 of Leishmania donovani modulates antimony susceptibility by downregulating P-glycoprotein efflux pumps.
P2860
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P2860
JNK activation is a mediator of arsenic trioxide-induced apoptosis in acute promyelocytic leukemia cells.
description
2003 nî lūn-bûn
@nan
2003 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2003 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
2003年の論文
@ja
2003年論文
@yue
2003年論文
@zh-hant
2003年論文
@zh-hk
2003年論文
@zh-mo
2003年論文
@zh-tw
2003年论文
@wuu
name
JNK activation is a mediator o ...... promyelocytic leukemia cells.
@ast
JNK activation is a mediator o ...... promyelocytic leukemia cells.
@en
JNK activation is a mediator o ...... promyelocytic leukemia cells.
@nl
type
label
JNK activation is a mediator o ...... promyelocytic leukemia cells.
@ast
JNK activation is a mediator o ...... promyelocytic leukemia cells.
@en
JNK activation is a mediator o ...... promyelocytic leukemia cells.
@nl
prefLabel
JNK activation is a mediator o ...... promyelocytic leukemia cells.
@ast
JNK activation is a mediator o ...... promyelocytic leukemia cells.
@en
JNK activation is a mediator o ...... promyelocytic leukemia cells.
@nl
P2093
P1433
P1476
JNK activation is a mediator o ...... promyelocytic leukemia cells.
@en
P2093
Kelly Davison
Koren K Mann
Wilson H Miller
P304
P356
10.1182/BLOOD-2003-05-1412
P407
P577
2003-12-30T00:00:00Z