The molecular control of DNA damage-induced cell death

Apoptosis

Volumn 5, Issue 6, 2000, Pages 491-507

  Coultas, Leigh ^a   Strasser, Andreas ^a  

^a WALTER AND ELIZA HALL INSTITUTE OF MEDICAL RESEARCH   (Australia)

Author keywords

Apoptosis; Bcl 2; Caspases; Death receptors; DNA damage; p53

Indexed keywords

CASPASE; CELL RECEPTOR; PROTEIN BCL 2; PROTEIN P53;

APOPTOSIS; CANCER THERAPY; CARCINOGENESIS; CELL CYCLE; CELL DEATH; DNA DAMAGE; DNA REPAIR; HUMAN; MOLECULAR BIOLOGY; NONHUMAN; PRIORITY JOURNAL; REGULATORY MECHANISM; REVIEW; SIGNAL TRANSDUCTION; TUMOR SUPPRESSOR GENE;

ANIMALS; APOPTOSIS; DNA DAMAGE; DRUG RESISTANCE, NEOPLASM; HUMANS; NEOPLASMS; SIGNAL TRANSDUCTION;

METAZOA;

EID: 0034475027     PISSN: 13608185     EISSN: None     Source Type: Journal    
DOI: 10.1023/A:1009617727938     Document Type: Review

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88. A novel protein that interacts with the death domain of Fas/APO1 contains a sequence motif related to the death domain
89. FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis
90. An induced proximity model for caspase-8 activation
91. Membrane oligomerization and cleavage activates the caspase-8 (FLICE/MACH1) death signal
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93. FLICE is activated by association with the CD95 death-inducing signaling complex (DISC)
94. A dominant interfering mutant of FADD/Mort1 enhances deletion of autoreactive thymocytes and inhibits proliferation of mature T lymphocytes
95. FADD: Essential for embryo development and signaling from some, but not all, inducers of apoptosis
96. Fasmediated apoptosis and activation-induced T-cell proliferation are defective in mice lacking FADD/Mort1
97. CrmA expression in T lymphocytes of transgenic mice inhibits CD95 (Fas/APO-1)transduced apoptosis, but does not cause lymphadenopathy or autoimmune disease
98. Targeted disruption of the mouse Caspase 8 gene ablates cell death induction by the TNF receptors, Fas/Apo1, and DR3 and is lethal prenatally
99. TRADD-TRAF2 and TRADD-FADD interactions define two distinct TNF Receptor 1 signal transduction pathways
100. TRAIL receptor-2 signals apoptosis through FADD and caspase-8
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102. FADD/MORT1 and caspase-8 are recruited to TRAIL receptors 1 and 2 and are essential for apoptosis mediated by TRAIL receptor 2
103. Effect of bcl-2 proto-oncogene expression on cellular sensitivity to tumor necrosis factor-mediated cytotoxicity
104. Bcl-2 and Fas/APO-1 regulate distinct pathways to lymphocyte apoptosis
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117. -/- mice
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128. Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC
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136. The pro-apoptotic activity of the Bcl-2 family member Bim is regulated by interaction with the dynein motor complex
137. Blocking apoptosis prevents blindness in Drosophila retinal degeneration mutants
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156. p53-mediated up-regulation of CD95 is not involved in genotoxic drug-induced apoptosis of human breast tumor cells
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158. Constitutive expression of Fas ligand in thyrocytes
159. Technical note: Aberrant detection of cell surface Fas ligand with anti-peptide antibodies
160. Specificity questions concerning the clone 33 anti-fas ligand antibody
161. mAb 33 from Transduction Laboratories specifically binds to human CD95L
162. Antibody mAb33 from Transduction Laboratories detects human CD95L in ELISA but not in immunoblots
163. Drug-induced apoptosis is associated with enhanced Fas (Apo-1/CD95) ligand expression but occurs independently of Fas (Apo-1/CD95) signaling in human T-acute lymphatic leukemia cells
164. Comparison of apoptosis in wild-type and Fas-resistant cells-Chemotherapy-induced apoptosis is not dependent on Fas/Fas ligand interactions
165. Myeloma cells selected for resistance to CD95-mediated apoptosis are not cross-resistant to cytotoxic drugs: Evidence for independent mechanisms of caspase activation
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168. Inhibition of death receptor signals by cellular FLIP
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170. FLIP prevents apoptosis induced by death receptors but not by perforin/granzyme B, chemotherapeutic drugs, and gamma irradiation
171. Fas ligand-induced c-Jun kinase activation in lymphoid cells requires extensive receptor aggregation but is independent of DAXX, and Fas-mediated cell death does not involve DAXX, RIP or RAIDD
172. Activation of a CrmA insensitive, p35-sensitive pathway in ionizing radiation-induced apoptosis
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178. CD95 (Fas/APO-1) and p53 signal apoptosis independently in diverse cell rypes
179. Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand
180. FADD/MORT1 regulates the pre-TCR checkpoint and can function as a tumour suppressor
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182. Systemic overexpression of BCL-2 in the hematopoietic system protects transgenic mice from the consequences of lethal irradiation
183. L displays restricted distribution during T cell development and inhibits multiple forms of apoptosis but not clonal deletion in transgenic mice
184. bcl-2 gene transfer increases relative resistance of S49.1 and WEHI17.2 lymphoid cells to cell death and DNA fragmentation induced by glucocorticoids and multiple chemotherapeutic drugs
185. bcl-w, a novel member of the bcl-2 family, promotes cell survival
186. L and adenovirus protein E1B19kD are functionally equivalent in their ability to inhibit cell death
187. Bcl-2-deficient mice demonstrate fulminant lymphoid apoptosis, polycystic kidneys, and hypopigmented hair
188. Bclx regulates the survival of double-positive thymocytes
189. Disappearance of the lymphoid system in Bcl-2 homozygous mutant chimeric mice
190. Bcl-w is an important determinant of damage-induced apoprosis in epithelia of small and large intestine
191. Wild-type p53-triggered apoptosis is inhibited by bcl-2 in a v-myc-induced T-cell lymphoma line
192. Bcl-2 blocks p53-dependent apoptosis
193. bfl-1, a bcl-2 homologue, suppresses p53-induced apoptosis and exhibits potent cooperative transforming activity
194. Overexpression of Bcl-2 in bladder cancer cells inhibits apoptosis induced by cisplatin and adenoviral-mediated p53 gene transfer
195. Bcl-2 blocks glucocorticoid- but not Fas- or activation-induced apoptosis in a T cell hybridoma
196. Bcl-2 blocks degranulation but not fas-based cell-mediated cytotoxicity
197. bcl-2 transgenic Lpr mice show profound enhancement of lymphadenopathy
198. Inhibition of apoptosis and augmentation of lymphoproliferation in bcl-2 transgenic Fas/Fas ligand-defective mice
199. Differential requirement for caspase 9 in apoptotic pathways in vivo
200. Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9
201. Tumor suppressor p53 is a direct transcriptional activator of the human bax gene
202. γ-radiation induces upregulation of Bax protein and apoptosis in radiosensitive cells in vivo
203. The activity of the murine bax promoter is regulated by Sp1/3 and E-box binding proteins but nor by p53
204. Bax-deficient mice with lymphoid hyperplasia and male germ cell death
205. T cells from baxα transgenic mice show accelerated apoptosis in response to stimuli but do not show restored DNA damage-induced cell death in the absence of p53
206. Atm and bax cooperate in ionizing radiation-induced apoptosis in the central nervous system
207. Noxa, a BH3-only member of the bcl-2 family and candidate mediator of p53-induced apoptosis
208. Activation of mouse lymphocytes inhibits induction of rapid cell death by X-irradiation
209. bcl-x, a bcl-2-related gene that functions as a dominant regulator of apoptotic cell death
210. B lymphocytes differentially use the Rel and nuclear factor κB1 (NF-κB1) transcription factors to regulate cell cycle progression and apoptosis in quiescent and mitogen-activated cells
211. Rel-dependent induction of A1 transcription is required to protect B cells from antigen receptor ligation-induced apoptosis
212. The pro-apoptotic BH3-only protein Bim is expressed in hemopoietic, epithelial, neuronal and germ cells
213. ATM in lymphoid development and tumorigenesis
214. Atm-deficient mice: A paradigm of ataxia telangiectasia
215. Pleiotropic defects in ataxia-telangiectasia protein-deficient mice
216. Critical role for Atm in suppressing V(D)J recombination-driven thymic lymphoma
217. DNA-PKcs: A T-cell tumour suppressor encoded at the mouse scid locus
218. Kn70: A candidate tumor suppressor gene for murine T cell lymphoma
219. DNA repair protein Ku80 suppresses chromosomal aberrations and malignant transformation
220. Lessons from hereditary colorectal cancer
221. Inactivation of the mouse Msb2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer
222. MSH2 deficient mice are viable and susceptible to lymphoid tumours
223. Male mice defective in the DNA mismatch repair gene PMS2 exhibit abnormal chromosome synapsis in meiosis
224. HNPCC-like cancer predisposition in mice through simultaneous loss of Msh3 and Msh6 mismatch-repair protein functions
225. Heterozygous germ line hCHK2 mutations in Li-Fraumeni syndrome
226. p53 mutations in human cancers
227. The p53 tumour suppressor gene
228. Germ line p53 mutations in a familial syndrome of breast cancer, sarcomas, and other neoplasms
229. Tumor spectrum analysis in p53-mutant mice
230. V(D)J recombination is not required for the development of lymphoma in p53-deficient mice
231. Progression from lymphoid hyperplasia to high-grade malignant lymphoma in mice transgenic for the t(14;18)
232. Eμ-bcl-2 transgene facilitates spontaneous transformation of early pre-B and immunoglobulin-secreting cells but not T cells
233. Peripheral T-cell lymphoma in lckpr-bcl-2 transgenic mice
234. Mediation of c-Myc-induced apoptosis by p53
235. Mutations in the p53 and SCID genes cooperate in tumorigenesis
236. V(D)J recombination activates a p53-dependent DNA damage checkpoint in scid lymphocyte precursors
237. Genetic interactions between atm and p53 influence cellular proliferation and irradiation-induced cell cycle checkpoints
238. A critical role for DNA end-joining proteins in both lymphogenesis and neurogenesis
239. DNA Ligase IV deficiency in mice leads to defective neurogenesis and embryonic lethality via the p53 pathway
240. Interplay of p53 and DNA-repair protein XRCC4 in tumorigenesis, genomic stability and development
241. p53-dependent apoptosis modulates the cytotoxicity of anticancer agents
242. Does 'death receptor'-signalling play a role in tumourigenesis and cancer therapy?
243. BMS-only proteins-essential initiators of apoptotic cell death