The kinase inhibitor sorafenib induces cell death through a process involving induction of endoplasmic reticulum stress.
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Modulation of Autophagy by Sorafenib: Effects on Treatment ResponseTargeting the Bcl-2 family for cancer therapyXenobiotic perturbation of ER stress and the unfolded protein responseTargeting Mcl-1 for the therapy of cancerCompound C prevents the unfolded protein response during glucose deprivation through a mechanism independent of AMPK and BMP signalingMcl-1 downregulation by pro-inflammatory cytokines and palmitate is an early event contributing to β-cell apoptosisReduced immunosuppressive properties of axitinib in comparison with other tyrosine kinase inhibitors.Inositol-requiring enzyme 1alpha is a key regulator of angiogenesis and invasion in malignant gliomaPhase II study of sorafenib in patients with relapsed or refractory lymphoma.Histone deacetylase inhibitors activate NF-kappaB in human leukemia cells through an ATM/NEMO-related pathwayPharmacological inhibition of cystine-glutamate exchange induces endoplasmic reticulum stress and ferroptosisA genome-wide RNA interference screen reveals an essential CREB3L2-ATF5-MCL1 survival pathway in malignant glioma with therapeutic implications.Bcl-2 antagonists interact synergistically with bortezomib in DLBCL cells in association with JNK activation and induction of ER stress.Sorafenib activates CD95 and promotes autophagy and cell death via Src family kinases in gastrointestinal tumor cells.Sorafenib: complexities of Raf-dependent and Raf-independent signaling are now unveiled.Sorafenib/regorafenib and lapatinib interact to kill CNS tumor cells.Stat5 regulates cellular iron uptake of erythroid cells via IRP-2 and TfR-1.Melanoma differentiation associated gene-7/interleukin-24 potently induces apoptosis in human myeloid leukemia cells through a process regulated by endoplasmic reticulum stress.Dinaciclib (SCH727965) inhibits the unfolded protein response through a CDK1- and 5-dependent mechanismA novel proteasome inhibitor acting in mitochondrial dysfunction, ER stress and ROS production.In vitro and in vivo interactions between the HDAC6 inhibitor ricolinostat (ACY1215) and the irreversible proteasome inhibitor carfilzomib in non-Hodgkin lymphoma cellsSorafenib synergizes with metformin in NSCLC through AMPK pathway activation.Inhibition of MEK/ERK1/2 sensitizes lymphoma cells to sorafenib-induced apoptosisMechanism by which Mcl-1 regulates cancer-specific apoptosis triggered by mda-7/IL-24, an IL-10-related cytokineIdentification of known drugs targeting the endoplasmic reticulum stress response.Gefitinib and Erlotinib Lead to Phosphorylation of Eukaryotic Initiation Factor 2 Alpha Independent of Epidermal Growth Factor Receptor in A549 CellsFADD cleavage by NK cell granzyme M enhances its self-association to facilitate procaspase-8 recruitment for auto-processing leading to caspase cascadeInhibition of Bcl-2 antiapoptotic members by obatoclax potently enhances sorafenib-induced apoptosis in human myeloid leukemia cells through a Bim-dependent processSuppression of PP2A is critical for protection of melanoma cells upon endoplasmic reticulum stress.Lapatinib and obatoclax kill breast cancer cells through reactive oxygen species-dependent endoplasmic reticulum stress.A combination of sorafenib and nilotinib reduces the growth of castrate-resistant prostate cancer.Autophagy-dependent EIF2AK3 activation compromises ursolic acid-induced apoptosis through upregulation of MCL1 in MCF-7 human breast cancer cells.A SPRY2 mutation leading to MAPK/ERK pathway inhibition is associated with an autosomal dominant form of IgA nephropathyNexavar/Stivarga and viagra interact to kill tumor cells.GRP78/Dna K Is a Target for Nexavar/Stivarga/Votrient in the Treatment of Human Malignancies, Viral Infections and Bacterial Diseases.Artemisinin-derived dimer ART-838 potently inhibited human acute leukemias, persisted in vivo, and synergized with antileukemic drugs.Vorinostat and sorafenib synergistically kill tumor cells via FLIP suppression and CD95 activation.Vemurafenib potently induces endoplasmic reticulum stress-mediated apoptosis in BRAFV600E melanoma cells.p21(Cip1) protects against oxidative stress by suppressing ER-dependent activation of mitochondrial death pathways.The Bruton tyrosine kinase (BTK) inhibitor PCI-32765 synergistically increases proteasome inhibitor activity in diffuse large-B cell lymphoma (DLBCL) and mantle cell lymphoma (MCL) cells sensitive or resistant to bortezomib.
P2860
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P2860
The kinase inhibitor sorafenib induces cell death through a process involving induction of endoplasmic reticulum stress.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
The kinase inhibitor sorafenib ...... endoplasmic reticulum stress.
@ast
The kinase inhibitor sorafenib ...... endoplasmic reticulum stress.
@en
type
label
The kinase inhibitor sorafenib ...... endoplasmic reticulum stress.
@ast
The kinase inhibitor sorafenib ...... endoplasmic reticulum stress.
@en
prefLabel
The kinase inhibitor sorafenib ...... endoplasmic reticulum stress.
@ast
The kinase inhibitor sorafenib ...... endoplasmic reticulum stress.
@en
P2093
P2860
P356
P1476
The kinase inhibitor sorafenib ...... endoplasmic reticulum stress.
@en
P2093
Eric Maynard Davis
Joseph Reza Habibi
Mohamed Rahmani
Steven Grant
Timothy Ryan Crabtree
Tri K Nguyen
P2860
P304
P356
10.1128/MCB.01080-06
P407
P50
P577
2007-06-04T00:00:00Z