Mouse models of cell death

Nature Genetics

Volumn 28, Issue 2, 2001, Pages 113-118

  Ranger, A M ^a   Malynn, B A ^a   Korsmeyer, S J ^a  

^a HOWARD HUGHES MEDICAL INSTITUTE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ADAPTOR PROTEIN; CASPASE; PROTEIN BCL 2;

APOPTOSIS; CAENORHABDITIS ELEGANS; CELL DEATH; DEVELOPMENTAL GENETICS; DROSOPHILA MELANOGASTER; GENETIC MODEL; HOMEOSTASIS; KNOCKOUT MOUSE; METAZOON; PHENOTYPE; PRIORITY JOURNAL; REGULATORY MECHANISM; REVIEW; TRANSGENIC MOUSE;

ANIMALS; ANTIGENS, CD; ANTIGENS, CD95; APOPTOSIS; APOPTOTIC PROTEASE-ACTIVATING FACTOR 1; BCL-X PROTEIN; CASPASES; CELL DEATH; MICE; MICE, KNOCKOUT; MITOCHONDRIA; PROTEINS; PROTO-ONCOGENE PROTEINS C-BCL-2; RECEPTORS, TUMOR NECROSIS FACTOR; RECEPTORS, TUMOR NECROSIS FACTOR, MEMBER 25; RECEPTORS, TUMOR NECROSIS FACTOR, TYPE I; SIGNAL TRANSDUCTION;

CAENORHABDITIS ELEGANS; DROSOPHILA MELANOGASTER; MAMMALIA; MELANOGASTER; METAZOA; MUS MUSCULUS;

EID: 0034975774     PISSN: 10614036     EISSN: None     Source Type: Journal    
DOI: 10.1038/88815     Document Type: Review

References (65)

1. Apoptosis: A basic biological phenomenon with wide-ranging implications in tissue kinetics
2. Cell death in development
3. A portrait of the Bcl-2 protein family: Life, death, and the whole picture
4. Mechanisms and functions of cell death
5. An emerging blueprint for apoptosis in Drosophila
6. Membrane oligomerization and cleavage activates the caspase-8 (FLICE/MACHalpha1) death signal
7. An induced proximity model for caspase-8 activation
8. Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade
9. BCL-2 family members and the mitochondria in apoptosis
10. tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c
11. Targeted disruption of the mouse Caspase 8 gene ablates cell death induction by the TNF receptors, Fas/Apo1, and DR3 and is lethal prenatally
12. FADD: Essential for embryo development and signaling from some, but not all, inducers of apoptosis
13. Fas-mediated apoptosis and activation-induced T-cell proliferation are defective in mice lacking FADD/Mort1
14. Requirement for Casper (c-FLIP) in regulation of death receptor-induced apoptosis and embryonic development
15. Defects in regulation of apoptosis in caspase-2-deficient mice
16. A dominant interfering mutant of FADD/MORT1 enhances deletion of autoreactive thymocytes and inhibits proliferation of mature T lymphocytes
17. FADD/MORT1 regulates the pre-TCR checkpoint and can function as a tumour suppressor
18. Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis
19. Caspase cleaved BID targets mitochondria and is required for cytochrome c release, while BCL-XL prevents this release but not tumor necrosis factor-R1/Fas death
20. Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis
21. Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis
22. Bcl-2 protein expression during murine development
23. bcl-2 protein expression is widespread in the developing nervous system and retained in the adult PNS
24. Bcl-2-deficient mice demonstrate fulminant lymphoid apoptosis, polycystic kidneys, and hypopigmented hair
25. bcl-XL is the major bcl-x mRNA form expressed during murine development and its product localizes to mitochondria
26. Massive cell death of immature hematopoietic cells and neurons in Bcl-x-deficient mice
27. Bclx regulates the survival of double-positive thymocytes
28. Apoptosis regulator bcl-w is essential for spermatogenesis but appears otherwise redundant
29. Testicular degeneration in Bclw-deficient mice
30. Mcl-1 deficiency results in peri-implantation embryonic lethality
31. Mcl-1 in transgenic mice promotes survival in a spectrum of hematopoietic cell types and immortalization in the myeloid lineage
32. Accelerated neutrophil apoptosis in mice lacking A1-a, a subtype of the bcl-2-related A1 gene
33. Proapoptotic Bcl-2 relative Bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity
34. Bax-deficient mice with lymphoid hyperplasia and male germ cell death
35. Bcl-2 and Bax function independently to regulate cell death
36. Widespread elimination of naturally occurring neuronal death in Bax-deficient mice
37. BAX is required for neuronal death after trophic factor deprivation and during development
38. Bax deletion further orders the cell death pathway in cerebellar granule cells and suggests a caspase-independent pathway to cell death
39. Prolongation of ovarian lifespan into advanced chronological age by Bax-deficiency
40. The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues
41. Pro-apoptotic BAX and BAK are a requisite gateway to mitochondrial dysfunction and death
42. Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-beta
43. Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis
44. Molecular characterization of mitochondrial apoptosis-inducing factor
45. Signals for death and survival: A two-step mechanism for cavitation in the vertebrate embryo
46. Essential role of the mitochondrial apoptosis-inducing factor in programmed cell death
47. IAP family proteins - Suppressors of apoptosis
48. Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition
49. Identification of DIABLO, a mammalian protein that promotes apoptosis by binding to and antagonizing IAP proteins
50. Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice
51. Essential contribution of caspase 3/CPP32 to apoptosis and its associated nuclear changes
52. Differential requirement for caspase 9 in apoptotic pathways in vivo
53. Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9
54. Apaf1 (CED-4 homolog) regulates programmed cell death in mammalian development
55. Apaf1 is required for mitochondrial pathways of apoptosis and brain development
56. Caspase-3 controls both cytoplasmic and nuclear events associated with Fas-mediated apoptosis in vivo
57. Deficiency in caspase-9 or caspase-3 induces compensatory caspase activation
58. In vivo evidence that caspase-3 is required for Fas-mediated apoptosis of hepatocytes
59. Mice deficient in IL-1 beta-converting enzyme are defective in production of mature IL-1 beta and resistant to endotoxic shock
60. Altered cytokine export and apoptosis in mice deficient in interleukin-1 beta converting enzyme
61. Dual role of caspase-11 in mediating activation of caspase-1 and caspase-3 under pathological conditions
62. Reduced ischemic brain injury in interleukin-1 beta converting enzyme-deficient mice
63. Murine caspase-11, an ICE-interacting protease, is essential for the activation of ICE
64. Adult Apaf-1-deficient mice exhibit male infertility
65. Inactivation of bcl-2 results in progressive degeneration of motoneurons, sympathetic and sensory neurons during early postnatal development