Understanding apoptosis by systems biology approaches

被引:37
作者
Lavrik, Inna N. [1 ]
Eils, Roland [2 ,3 ]
Fricker, Nicolai [1 ]
Pforr, Carina [1 ]
Krammer, Peter H. [1 ]
机构
[1] German Canc Res Ctr, Div Immunogenet, D-69120 Heidelberg, Germany
[2] German Canc Res Ctr, Div Theoret Bioinformat, D-69120 Heidelberg, Germany
[3] Heidelberg Univ, Dept Bioinformat & Funct Genom, Inst Pharm & Mol Biotechnol, D-69120 Heidelberg, Germany
关键词
CASPASE ACTIVATION; DEATH; MODEL; PROTEIN; BCL-2; BISTABILITY; INHIBITOR; REGULATOR; DOMAIN; SWITCH;
D O I
10.1039/b905129p
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Apoptosis is a process common to all multicellular organisms. Apoptosis leads to the elimination of cells via a complex but highly defined cellular programme. Defects in the regulation of apoptosis result in serious diseases such as cancer, autoimmunity, AIDS and neurodegeneration. Recently, a substantial step forward in understanding the complex apoptotic pathways has been made by utilising systems biology approaches. Systems biology combines rigorous mathematical modelling with experimental approaches in a closed loop cycle for advancing our knowledge about complex biological processes. In this review we describe the contemporary systems biology studies devoted to apoptotic signalling and focus on the question of how systems biology helps to understand life/death decisions made in the cell and to develop new approaches to rational treatment strategies.
引用
收藏
页码:1105 / 1111
页数:7
相关论文
共 40 条
  • [11] X-linked IAP is a direct inhibitor of cell-death proteases
    Deveraux, QL
    Takahashi, R
    Salvesen, GS
    Reed, JC
    [J]. NATURE, 1997, 388 (6639) : 300 - 304
  • [12] Bistability analyses of a caspase activation model for receptor-induced apoptosis
    Eissing, T
    Conzelmann, H
    Gilles, ED
    Allgöwer, F
    Bullinger, E
    Scheurich, P
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (35) : 36892 - 36897
  • [13] Stochastic modelling of apoptosis kinetics
    Fennell, DA
    Pallaska, A
    Corbo, M
    Cotter, FE
    [J]. APOPTOSIS, 2005, 10 (02) : 447 - 452
  • [14] The protein structures that shape caspase activity, specificity, activation and inhibition
    Fuentes-Prior, P
    Salvesen, GS
    [J]. BIOCHEMICAL JOURNAL, 2004, 384 : 201 - 232
  • [15] A mathematical model of caspase function in apoptosis
    Fussenegger, M
    Bailey, JE
    Varner, J
    [J]. NATURE BIOTECHNOLOGY, 2000, 18 (07) : 768 - 774
  • [16] c-FLIPR, a new regulator of death receptor-induced apoptosis
    Golks, A
    Brenner, D
    Fritsch, C
    Krammer, PH
    Lavrik, IN
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (15) : 14507 - 14513
  • [17] The pathophysiology of mitochondrial cell death
    Green, DR
    Kroemer, G
    [J]. SCIENCE, 2004, 305 (5684) : 626 - 629
  • [18] Effects of Bcl-2 levels on Fas signaling-induced caspase-3 activation: Molecular genetic tests of computational model predictions
    Hua, F
    Cornejo, MG
    Cardone, MH
    Stokes, CL
    Lauffenburger, DA
    [J]. JOURNAL OF IMMUNOLOGY, 2005, 175 (02) : 985 - 995
  • [19] Systems model of signaling identifies a molecular basis set for cytokine-induced apoptosis
    Janes, KA
    Albeck, JG
    Gaudet, S
    Sorger, PK
    Lauffenburger, DA
    Yaffe, MB
    [J]. SCIENCE, 2005, 310 (5754) : 1646 - 1653
  • [20] Systems biology: A brief overview
    Kitano, H
    [J]. SCIENCE, 2002, 295 (5560) : 1662 - 1664