ApoptoProteomics, an Integrated Database for Analysis of Proteomics Data Obtained from Apoptotic Cells

被引:31
作者
Arntzen, Magnus O. [1 ,2 ,3 ,4 ]
Thiede, Bernd [1 ]
机构
[1] Univ Oslo, Biotechnol Ctr Oslo, N-0317 Oslo, Norway
[2] Natl Hosp Norway, Oslo Univ Hosp, Prote Core Facil, N-0027 Oslo, Norway
[3] Univ Oslo, N-0027 Oslo, Norway
[4] Norwegian Univ Life Sci, Prote Core Facil, N-1432 As, Norway
关键词
CLEAVAGE SITES; INTERMEDIATE-FILAMENTS; CASPASE CLEAVAGE; PROTEIN; PREDICTION; MECHANISMS; PROTEASOME; REORGANIZATION; DROSOPHILA; CYTOSCAPE;
D O I
10.1074/mcp.M111.010447
中图分类号
Q5 [生物化学];
学科分类号
071010 ; 081704 ;
摘要
Apoptosis is the most commonly described form of programmed cell death, and dysfunction is implicated in a large number of human diseases. Many quantitative proteome analyses of apoptosis have been performed to gain insight in proteins involved in the process. This resulted in large and complex data sets that are difficult to evaluate. Therefore, we developed the ApoptoProteomics database for storage, browsing, and analysis of the outcome of large scale proteome analyses of apoptosis derived from human, mouse, and rat. The proteomics data of 52 publications were integrated and unified with protein annotations from UniProt-KB, the caspase substrate database homepage (CASBAH), and gene ontology. Currently, more than 2300 records of more than 1500 unique proteins were included, covering a large proportion of the core signaling pathways of apoptosis. Analysis of the data set revealed a high level of agreement between the reported changes in directionality reported in proteomics studies and expected apoptosis-related function and may disclose proteins without a current recognized involvement in apoptosis based on gene ontology. Comparison between induction of apoptosis by the intrinsic and the extrinsic apoptotic signaling pathway revealed slight differences. Furthermore, proteomics has significantly contributed to the field of apoptosis in identifying hundreds of caspase substrates. The database is available at http://apoptoproteomics.uio.no. Molecular & Cellular Proteomics 11: 10.1074/mcp.M111.010447, 1-15, 2012.
引用
收藏
页数:15
相关论文
共 67 条
[1]   Caspase-dependent inactivation of proteasome function during programmed cell death in Drosophila and man [J].
Adrain, C ;
Creagh, EM ;
Cullen, SP ;
Martin, SJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (35) :36923-36930
[2]   GraBCas: a bioinformatics tool for score-based prediction of caspase- and granzyme B-cleavage sites in protein sequences [J].
Backes, C ;
Kuentzer, J ;
Lenhof, HP ;
Comtesse, N ;
Meese, E .
NUCLEIC ACIDS RESEARCH, 2005, 33 :W208-W213
[3]   Rearrangement of nuclear ribonucleoprotein (RNP)-containing structures during apoptosis and transcriptional arrest [J].
Biggiogera, M ;
Bottone, MG ;
Scovassi, AI ;
Soldani, C ;
Vecchio, L ;
Pellicciari, C .
BIOLOGY OF THE CELL, 2004, 96 (08) :603-615
[4]   Regulation of the Apaf-1-caspase-9 apoptosome [J].
Bratton, Shawn B. ;
Salvesen, Guy S. .
JOURNAL OF CELL SCIENCE, 2010, 123 (19) :3209-3214
[5]   Caspase cleavage of vimentin disrupts intermediate filaments and promotes apoptosis [J].
Byun, Y ;
Chen, F ;
Chang, R ;
Trivedi, M ;
Green, KJ ;
Cryns, VL .
CELL DEATH AND DIFFERENTIATION, 2001, 8 (05) :443-450
[6]   Cytosolic accumulation of HSP60 during apoptosis with or without apparent mitochondrial release - Evidence that its pro-apoptotic or pro-survival functions involve differential interactions with caspase [J].
Chandra, Dhyan ;
Choy, Grace ;
Tang, Dean G. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2007, 282 (43) :31289-31301
[7]  
Chu JJ, 1998, J CELL BIOCHEM, V68, P472, DOI 10.1002/(SICI)1097-4644(19980315)68:4<472::AID-JCB7>3.3.CO
[8]  
2-P
[9]   Global mapping of the topography and magnitude of proteolytic events in apoptosis [J].
Dix, Melissa M. ;
Simon, Gabriel M. ;
Cravatt, Benjamin F. .
CELL, 2008, 134 (04) :679-691
[10]   The Oncoprotein SF2/ASF Promotes Non-Small Cell Lung Cancer Survival by Enhancing Survivin Expression [J].
Ezponda, Teresa ;
Pajares, Maria J. ;
Agorreta, Jackeline ;
Echeveste, Jose I. ;
Lopez-Picazo, Jose M. ;
Torre, Wenceslao ;
Pio, Ruben ;
Montuenga, Luis M. .
CLINICAL CANCER RESEARCH, 2010, 16 (16) :4113-4125