Nucleocytoplasmic shuttling of BID is involved in regulating its activities in the DNA-damage response

Cell Death and Differentiation

Volumn 14, Issue 9, 2007, Pages 1628-1634

  Oberkovitz, G ^a   Regev, L ^a   Gross, A ^a  

^a WEIZMANN INSTITUTE OF SCIENCE   (Israel)

Author keywords

[No Author keywords available]

Indexed keywords

ETOPOSIDE; EXPORTIN 1; LEPTOMYCIN B; PROTEIN BID;

APOPTOSIS; ARTICLE; CELL CYCLE ARREST; CELL CYCLE S PHASE; CELL DEATH; CELL NUCLEUS; CONSENSUS SEQUENCE; CONTROLLED STUDY; CYTOPLASM; DNA DAMAGE; HELA CELL; HUMAN; HUMAN CELL; IONIZING RADIATION; NUCLEAR EXPORT SIGNAL; NUCLEAR LOCALIZATION SIGNAL; NUCLEOCYTOPLASMIC TRANSPORT; PRIORITY JOURNAL; PROTEIN FUNCTION; PROTEIN LOCALIZATION; PROTEIN MOTIF; PROTEIN PHOSPHORYLATION; WILD TYPE;

ACTIVE TRANSPORT, CELL NUCLEUS; ANIMALS; BH3 INTERACTING DOMAIN DEATH AGONIST PROTEIN; CASPASES; CELL DEATH; CELL LINE; CELL NUCLEUS; DNA DAMAGE; ETOPOSIDE; HELA CELLS; HUMANS; MICE; MICROSCOPY, CONFOCAL; NUCLEAR LOCALIZATION SIGNALS; RECOMBINANT FUSION PROTEINS; S PHASE;

EID: 34548031619     PISSN: 13509047     EISSN: 14765403     Source Type: Journal    
DOI: 10.1038/sj.cdd.4402181     Document Type: Article

References (29)

1. Shi Y. Mechanisms of caspase activation and inhibition during apoptosis. Mol Cell 2002; 9: 459-470.
2. Daniel NN, Korsmeyer S.J. Cell death: Critical control points. Cell 2004; 116: 205-219.
3. Hockenbery D, Nunez G, Millman C, Schreiber RD, Korsmeyer SJ. Bcl-2 is an inner mitochondrial membrane protein that blocks programmed cell death. Nature 1990: 348: 334-338.
4. Krajewski S, Tanaka S, Takayama S, Schibler W, Fenton W, Reed JC. Investigation of the subcellular distribution of the bcl-2 oncoprotein: residence in the nuclear envelope, endoplasmic reticulum, and outer mitochondrial membranes. Cancer Res 1993; 53: 4701-4714.
5. Griffiths GJ, Dubrez L, Morgan CP, Jones NA, Whitehouse J, Corfe BM et al. Cell damage-induced conformational changes of the pro-apoptotic protein Bak in vivo precede the onset of apoptosis. J Cell Biol 1999; 144: 903-914.
6. Hsu YT, Wolter KG, Youle RJ. Cylosel-to-membrane redistribution of Bax and Bcl-X(L) during apoptosis. Proc Natl Acad Sci USA 1997; 94 3668-3672.
7. Gross A, Jockel J, Wei MC, Korsmeyer SJ. Enforced dimerization of BAX results in its translocation. mitochondrial dysfunction and apoptosis. EMBO J 1998; 17: 3878-3885.
8. Zha J, Harada H, Yang E, Jockel J, Korsmeyer SJ. Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L). Cell 1996; 87: 619-628.
9. Puthalakath H, Huang DC, O'Reilly LA, King SM, Strasser A. The proapoptotic activity of the Bcl-2 family member Bim is regulated by interaction with the dynein motor complex. Mol Cell 1999: 3: 287-296.
10. Wang X. The expanding role of mitochondria in apoptosis. Genes Dev 2001; 15: 2922-2933.
11. Willis SN, Adams JM. Life in the balance: How BH3-only proteins induce apoptosis. Curr Opin Cell Biol 2005; 17: 617-625.
12. Yin XM, Wang K, Gross A, Zhao Y, Zinkel S, Klocke B et al. Bid-deficient mice am resistant to Fas-induced hepatcellular apoptosis. Nature 1999; 400: 886-891.
13. Zinkel SS, Ong CC, Ferguson DO, Iwasaki H. Akashi K, Bronson RT et al. Proapoptotic BID is required for myeloid homeostasis and tumor suppression. Genes Dev 2003; 17: 229-239.
14. Gross A, McDonnell JM, Korsmeyer SJ. BCL-2 family members and the mitochondria in apoptosis. Genes Dev 1999; 13: 1899-1911.
15. Desagher S, Osen-Sand A, Nichols A, Eskes R, Montessuit S, Lauper S et al. Bid-induced conformational charge of Bax is responsible for mitochondrial cytochrome c release during apoptosis. J Cell Biol 1999; 144: 891-901.
16. Tefani M, Karpinich NO, Hurster KA, Pastorino JG, Schneider T, Russo MA et al. Cytochrome c release upon Fas receptor activation depends on translocation of full-length bid and the Induction of the mitochondrial permeability transition. J Biol Chem 2002; 277 10073-10082.
17. Sarig P, Zallsman Y, Marcellus RC, Flavel R, Mak TW, Gross A. BID-D59A is a potent inducer of apoptosis in primary embryonic fibroblast. J Biol Chem 2003; 278: 10707-10715.
18. Valentijn AJ, Gilmore AP. Translocation of full-length Bid to mitochondria during anoikis. J Biol Chem 2004; 279: 32848-32857.
19. Kamer I, Sarig R, Zaltsman Y, Niv H, Oberkovitz G, Regev L et al. Proapoptotic BID is an ATM effector in the DNA-damage response. Cell 2005; 122: 593-603.
20. Zinkel SS, Hurov KE, Ong C, Abtahi FM, Gross A, Korsmeyer S.J. A role for proapoptotic. BID in the DNA-damage response. Cell 2005; 122: 579-591.
21. Shiloh Y. The ATM-mediated DNA-damage response: Taking shape. Trends Biochem Sci 2006; 31: 402-410.
22. Gross A. BID as a double agent in cell life and death. Cell Cycle 2006; 5: 582-584.
23. Wolff B, Sanglier JJ, Wang Y. Leptomycin B is an inhibitor of nuclear export: Inhibition of nucleo-cytoplasmic translocation of the human immunodeficiency virus type 1 (HIV-1) Rev protein and Rev-dependent mRNA. Chem Biol 1997; 4: 139-147.
24. Henderson BR, Eleftheriou A. A comparison of the activity, sequence specificity, and CRM1-dependence of different nuclear export signals. Exp Cell Res 2000; 256: 213-224.
25. Nigg EA. Nucleocytoplasmic transport: Signals, mechanism and regulation. Nature 1997; 386: 779-787.
26. Kalderon D, Richardson WD, Markham AF, Smith AE. Sequence requirements for nuclear location of simian virus 40 large-T antigen. Nature 1984; 311: 33-38.
27. Lukas C, Falck J, Burtkova J, Bartek J, Lukas J. Distinct spatiotemporal dynamics of mammalian checkpoint regulators induced by DNA damage, Nat Cell Biol 2003; 5: 255-260.
28. Yu Y, Maggi Jr LB, Brady SN, Apicelli AJ, Dai MS, Lu H et al. Nucleophosmin-is essential for ribosomal protein L5 nuclear export. Mol Cell Biol 2006; 26: 3798-3809.
29. Tripathi AK, Chaturvedi R, Ahmad R, Asim M, Sawiari KK, Singh MK et al. Flow cytometric analysis of aneuploidy and S-phase fraction in chronic myeloid leukemia patients: Role in early detection of accelerated phase. Leuk Res 2003; 27: 899-902.