Implication of mitochondria-derived reactive oxygen species, cytochrome C and caspase-3 in N-(4-hydroxyphenyl)retinamide-induced apoptosis in cervical carcinoma cells.
about
Killing tumours by ceramide-induced apoptosis: a critique of available drugsDihydroorotate dehydrogenase is required for N-(4-hydroxyphenyl)retinamide-induced reactive oxygen species production and apoptosisSignal transduction of nitric oxide donor-induced protection in hydrogen peroxide-mediated apoptosis in H9C2 cardiomyoblasts.Fenretinide-induced apoptosis of Huh-7 hepatocellular carcinoma is retinoic acid receptor beta dependent.Selective apoptosis induction by the cancer chemopreventive agent N-(4-hydroxyphenyl)retinamide is achieved by modulating mitochondrial bioenergetics in premalignant and malignant human prostate epithelial cells.N-(4-hydroxyphenyl)retinamide-induced apoptosis triggered by reactive oxygen species is mediated by activation of MAPKs in head and neck squamous carcinoma cellsBursopentin (BP5) protects dendritic cells from lipopolysaccharide-induced oxidative stress for immunosuppression.Apoptosis as a novel target for cancer chemoprevention.Mitochondria: redox metabolism and dysfunction.Mitochondrial Malfunctioning, Proteasome Arrest and Apoptosis in Cancer Cells by Focused Intracellular Generation of Oxygen Radicals.Fenretinide stimulates redox-sensitive ceramide production in breast cancer cells: potential role in drug-induced cytotoxicity.Dihydroceramide accumulation and reactive oxygen species are distinct and nonessential events in 4-HPR-mediated leukemia cell death.Vitamin A depletion causes oxidative stress, mitochondrial dysfunction, and PARP-1-dependent energy deprivationBcl-2 family proteins as regulators of oxidative stress.Alveolar epithelial and endothelial cell apoptosis in emphysema: what we know and what we need to know.The dysfunction of the trabecular meshwork during glaucoma course.Implication of mitochondria-derived ROS and cardiolipin peroxidation in N-(4-hydroxyphenyl)retinamide-induced apoptosisUpregulation of GADD153 expression in the apoptotic signaling of N-(4-hydroxyphenyl)retinamide (4HPR).All-trans-retinoic acid induces manganese superoxide dismutase in human neuroblastoma through NF-kappaB.Clinically Evaluated Cancer Drugs Inhibiting Redox Signaling.Autophagy inhibition enhances isorhamnetin‑induced mitochondria‑dependent apoptosis in non‑small cell lung cancer cells.Reactive oxygen species are generated by the respiratory complex II--evidence for lack of contribution of the reverse electron flow in complex I.Increased mitochondrial DNA induces acquired docetaxel resistance in head and neck cancer cells.Evidence supporting a role for calcium in apoptosis induction by the synthetic triterpenoid 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO).Mitochondrial cytochrome c release mediates ceramide-induced activator protein 2 activation and gene expression in keratinocytes.Elucidation of molecular events mediating induction of apoptosis by synthetic retinoids using a CD437-resistant ovarian carcinoma cell line.Fenretinide induces mitochondrial ROS and inhibits the mitochondrial respiratory chain in neuroblastoma.Role of glutathione S-transferases in protection against lipid peroxidation. Overexpression of hGSTA2-2 in K562 cells protects against hydrogen peroxide-induced apoptosis and inhibits JNK and caspase 3 activation.Loss of MKP-5 promotes myofiber survival by activating STAT3/Bcl-2 signaling during regenerative myogenesis.Mitochondrial respiration is uniquely associated with the prooxidant and apoptotic effects of N-(4-hydroxyphenyl)retinamide.Cytochrome c oxidase subunit III: a molecular marker for N-(4-hydroxyphenyl)retinamise-induced oxidative stress in hepatoma cells.Sophoranone, extracted from a traditional Chinese medicine Shan Dou Gen, induces apoptosis in human leukemia U937 cells via formation of reactive oxygen species and opening of mitochondrial permeability transition pores.Cyclosporin A enhances the apoptotic effects of N-(4-hydroxyphenyl)retinamide in breast cancer cells.Fenretinide induces cytochrome c release, caspase 9 activation and apoptosis in the absence of mitochondrial membrane depolarisation.PPAR activation and decreased proliferation in oral carcinoma cells with 4-HPR.Redox cycling of Cu(II) by 6-mercaptopurine leads to ROS generation and DNA breakage: possible mechanism of anticancer activity.Toxicity of copper on isolated liver mitochondria: impairment at complexes I, II, and IV leads to increased ROS production.Reactive oxygen species mediate N-(4-hydroxyphenyl)retinamide-induced cell death in malignant T cells and are inhibited by the HTLV-I oncoprotein Tax.
P2860
Q24529892-DA2D54A4-D201-4E77-9F41-901E7F9BB2AFQ28279963-466E778B-A4F7-439A-AA74-100CF2C95598Q33182142-2A42734C-2B1C-4893-911B-1D5278E8EA9BQ33312870-8997BED4-5FF9-4CCD-9845-2DC68AC88ABDQ33935925-E0DA4A0A-3A4F-4F20-8645-2D20E982AAF1Q34594976-7AB726DA-563E-42AB-8B7C-3EDD8BF82F6BQ35557207-99465516-7BB3-4FFF-89AB-D07DDE701B02Q35764217-FFB0BF20-00BC-45B2-A84D-78CD115CD139Q35944831-58096C7E-034C-47AA-AE9A-9E2C89AF1850Q36183959-595C9402-5EA3-4494-8F11-617C1C436828Q36696260-BB800F72-1E5A-48E3-8CEE-B353B5FF0647Q36874463-A5EBFF12-826C-40CB-829C-277F22CEF289Q36950983-438B6D22-A796-4D2B-9B8A-957CD66BE88BQ37367025-8376672D-246A-4E73-8D41-7C9E884754B1Q37479097-05ABD3F3-9065-4E46-BF56-D4942AA2B264Q38248658-C8192774-2AFF-477E-8D1F-4C54ADF3D6ACQ38283683-101042A6-EEE1-4956-9B74-C056761FB443Q38362494-A3B0E97D-DBF2-48EE-85B4-B4E4A1523D52Q38663096-40959B9D-2A2C-43FD-8F4A-2F93558B5D5AQ38777221-8856E30E-C1D0-4BBA-A2A4-896E0503EF1CQ38846752-D26A9B4F-21B8-4A2B-B63F-339682FA01A3Q39233625-109FACC7-F61F-43CE-A353-FE6C7B26DB55Q40105899-C979E53D-313F-4A7D-81B9-779471386A4BQ40601361-E623F16F-8648-49EC-B5D4-8A62EE159BEAQ40638238-35AAE2D4-F843-45AA-8A34-B87CEE698BD6Q40703405-6CC856A5-FCD2-4D6D-9BDA-2C5B1D433A6DQ42073904-8A7FFF1B-AC99-45D0-85DB-172D177A2574Q42502038-B24FF9DE-2E05-4191-8A27-0DA0D215257AQ42672321-19A22BBA-C8C1-4438-960D-CAFF1FBDEAE6Q43730389-FA1A5D44-FD4D-467A-B3E3-A00C169420BDQ43792252-FD80DD11-8560-486E-977F-4770C2EFCB3BQ44062492-1842E636-1CF3-40AF-BFFD-ABB674B7380DQ44124427-70721046-9578-4CC9-9E71-9C122E70937EQ44483601-E3933011-4897-4109-8861-9649B60C81CEQ46794172-0075641C-6B24-4716-855D-C75593816DE4Q46821737-860C3E11-4799-4B2B-80FA-7A3090156160Q46911059-690A1487-8595-4017-B825-BEA5D2FE1312Q55239415-15175A69-B485-441E-84DE-F3C4DF13AA8B
P2860
Implication of mitochondria-derived reactive oxygen species, cytochrome C and caspase-3 in N-(4-hydroxyphenyl)retinamide-induced apoptosis in cervical carcinoma cells.
description
1999 nî lūn-bûn
@nan
1999年の論文
@ja
1999年学术文章
@wuu
1999年学术文章
@zh
1999年学术文章
@zh-cn
1999年学术文章
@zh-hans
1999年学术文章
@zh-my
1999年学术文章
@zh-sg
1999年學術文章
@yue
1999年學術文章
@zh-hant
name
Implication of mitochondria-de ...... s in cervical carcinoma cells.
@en
Implication of mitochondria-de ...... s in cervical carcinoma cells.
@nl
type
label
Implication of mitochondria-de ...... s in cervical carcinoma cells.
@en
Implication of mitochondria-de ...... s in cervical carcinoma cells.
@nl
prefLabel
Implication of mitochondria-de ...... s in cervical carcinoma cells.
@en
Implication of mitochondria-de ...... s in cervical carcinoma cells.
@nl
P2093
P2860
P356
P1433
P1476
Implication of mitochondria-de ...... s in cervical carcinoma cells.
@en
P2093
P2860
P2888
P304
P356
10.1038/SJ.ONC.1203024
P407
P577
1999-11-01T00:00:00Z