Bortezomib-induced sensitization of malignant human glioma cells to vorinostat-induced apoptosis depends on reactive oxygen species production, mitochondrial dysfunction, Noxa upregulation, Mcl-1 cleavage, and DNA damage.
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Pazopanib and HDAC inhibitors interact to kill sarcoma cells.Inhibition of phosphatidylinositol 3-kinase/AKT signaling by NVP-BKM120 promotes ABT-737-induced toxicity in a caspase-dependent manner through mitochondrial dysfunction and DNA damage response in established and primary cultured glioblastoma cells.Targeting poly (ADP-ribose) polymerase partially contributes to bufalin-induced cell death in multiple myeloma cells.Nuclear translocation of B-cell-specific transcription factor, BACH2, modulates ROS mediated cytotoxic responses in mantle cell lymphoma.Dinaciclib, a Cyclin-Dependent Kinase Inhibitor Promotes Proteasomal Degradation of Mcl-1 and Enhances ABT-737-Mediated Cell Death in Malignant Human Glioma Cell Lines.ABT-737 synergizes with bortezomib to induce apoptosis, mediated by Bid cleavage, Bax activation, and mitochondrial dysfunction in an Akt-dependent context in malignant human glioma cell lines.Cucurbitacin-I inhibits Aurora kinase A, Aurora kinase B and survivin, induces defects in cell cycle progression and promotes ABT-737-induced cell death in a caspase-independent manner in malignant human glioma cellsInduction of cell death by the novel proteasome inhibitor marizomib in glioblastoma in vitro and in vivoBortezomib-mediated down-regulation of telomerase and disruption of telomere homeostasis contributes to apoptosis of malignant cells.TIC10/ONC201 synergizes with Bcl-2/Bcl-xL inhibition in glioblastoma by suppression of Mcl-1 and its binding partners in vitro and in vivo.NADPH oxidase biology and the regulation of tyrosine kinase receptor signaling and cancer drug cytotoxicitySurvivin inhibitor YM-155 sensitizes tumor necrosis factor- related apoptosis-inducing ligand-resistant glioma cells to apoptosis through Mcl-1 downregulation and by engaging the mitochondrial death pathwayEpigenetics and ncRNAs in brain function and disease: mechanisms and prospects for therapy.Therapeutic potential and functional interaction of carfilzomib and vorinostat in T-cell leukemia/lymphoma.DNA repair gene XRCC4 codon 247 polymorphism modified diffusely infiltrating astrocytoma risk and prognosis.Inhibition of homologous recombination with vorinostat synergistically enhances ganciclovir cytotoxicity.Histone deacetylase inhibitors restore toxic BH3 domain protein expression in anoikis-resistant mammary and brain cancer stem cells, thereby enhancing the response to anti-ERBB1/ERBB2 therapy.Modulation of Mcl-1 sensitizes glioblastoma to TRAIL-induced apoptosisHDAC inhibitors enhance the lethality of low dose salinomycin in parental and stem-like GBM cellsMechanisms of proteasome inhibitor-induced cytotoxicity in malignant glioma.Targeting of histone deacetylases in brain tumors.Nuclear factor-κB in glioblastoma: insights into regulators and targeted therapy.A NOXA/MCL-1 Imbalance Underlies Chemoresistance of Malignant Rhabdoid Tumor Cells.Co-administration of ABT-737 and SAHA induces apoptosis, mediated by Noxa upregulation, Bax activation and mitochondrial dysfunction in PTEN-intact malignant human glioma cell lines.Mcl-1 regulates reactive oxygen species via NOX4 during chemotherapy-induced senescence.Mitochondrial dysfunction RAD51, and Ku80 proteolysis promote apoptotic effects of Dinaciclib in Bcl-xL silenced cells.The ubiquitin-proteasome pathway in adult and pediatric brain tumors: biological insights and therapeutic opportunities.Survivin inhibitor YM155 induces mitochondrial dysfunction, autophagy, DNA damage and apoptosis in Bcl-xL silenced glioma cell lines.HDAC inhibitor PAC-320 induces G2/M cell cycle arrest and apoptosis in human prostate cancer.Therapeutic Potential of Thymoquinone in Glioblastoma Treatment: Targeting Major Gliomagenesis Signaling Pathways.Counteracting survival functions of EBNA3C in Epstein-Barr virus (EBV)-driven lymphoproliferative diseases by combination of SAHA and bortezomib.
P2860
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P2860
Bortezomib-induced sensitization of malignant human glioma cells to vorinostat-induced apoptosis depends on reactive oxygen species production, mitochondrial dysfunction, Noxa upregulation, Mcl-1 cleavage, and DNA damage.
description
2011 nî lūn-bûn
@nan
2011 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի նոյեմբերին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Bortezomib-induced sensitizati ...... cl-1 cleavage, and DNA damage.
@ast
Bortezomib-induced sensitizati ...... cl-1 cleavage, and DNA damage.
@en
type
label
Bortezomib-induced sensitizati ...... cl-1 cleavage, and DNA damage.
@ast
Bortezomib-induced sensitizati ...... cl-1 cleavage, and DNA damage.
@en
prefLabel
Bortezomib-induced sensitizati ...... cl-1 cleavage, and DNA damage.
@ast
Bortezomib-induced sensitizati ...... cl-1 cleavage, and DNA damage.
@en
P2093
P2860
P356
P1476
Bortezomib-induced sensitizati ...... cl-1 cleavage, and DNA damage.
@en
P2093
Daniel R Premkumar
Esther P Jane
Ian F Pollack
Joseph D DiDomenico
Naomi R Agostino
P2860
P304
P356
10.1002/MC.21835
P577
2011-11-15T00:00:00Z