Intrinsically Disordered Proteins in Bcl-2 Regulated Apoptosis

被引：59

作者：

Rautureau, Gilles J. P. ^{[1
]}

Day, Catherine L. ^{[2
]}

Hinds, Mark G. ^{[1
]}

机构：

[1] Walter & Eliza Hall Inst Med Res, Parkville, Vic 3052, Australia

[2] Univ Otago, Dept Biochem, Dunedin 9054, New Zealand

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2010年 / 11卷 / 04期

关键词：

apoptosis; Bcl-2; BH3-only; intrinsically disordered protein; protein structure; CELL-DEATH MACHINERY; DYNEIN LIGHT-CHAIN; BH3-ONLY PROTEINS; FAMILY-MEMBERS; MITOCHONDRIAL-MEMBRANE; UNSTRUCTURED PROTEINS; SIGNALING PATHWAY; CRYSTAL-STRUCTURE; INDUCE APOPTOSIS; STRUCTURAL BASIS;

D O I：

10.3390/ijms11041808

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：

Intrinsic cell death is mediated by interaction between pro-apoptotic and prosurvival proteins of the B-cell lymphoma-2 (Bcl-2) family. Members of this family are either intrinsically disordered or contain intrinsically disordered regions/domains that are critical to their function. Alternate splicing and post-translational modifications can determine the extent of these disordered regions and are critical for regulating Bcl-2 proteins. Conformational plasticity and structural transitions characterize the interactions within the Bcl-2 family, with conserved sequence motifs on both binding partners required for their molecular recognition.

引用

页码：1808 / 1824

页数：17

共 95 条

[1] Nomenclature of dynein light chain-linked BH3-only protein Bim isoforms [J].

Adachi, M ;

Zhao, X ;

Imai, K .

CELL DEATH AND DIFFERENTIATION, 2005, 12 (02) :192-193

[2] Alternative splicing of Bcl-2-related genes: functional consequences and potential therapeutic applications [J].

Akgul, C ;

Moulding, DA ;

Edwards, SW .

CELLULAR AND MOLECULAR LIFE SCIENCES, 2004, 61 (17) :2189-2199

[3] How do Bax and Bak lead to permeabilization of the outer mitochondrial membrane? [J].

Antignani, Antonella ;

Youle, Richard J. .

CURRENT OPINION IN CELL BIOLOGY, 2006, 18 (06) :685-689

[4] Phylogenomics of life-or-death switches in multicellular animals: Bcl-2, BH3-only, and BNip families of apoptotic regulators [J].

Aouacheria, A ;

Brunet, F ;

Gouy, M .

MOLECULAR BIOLOGY AND EVOLUTION, 2005, 22 (12) :2395-2416

[5] Crystal structure of rat Bcl-x(L) - Implications for the function of the Bcl-2 protein family [J].

Aritomi, M ;

Kunishima, N ;

Inohara, N ;

Ishibashi, Y ;

Ohta, S ;

Morikawa, K .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (44) :27886-27892

[6] MCL-1S, a splicing variant of the antiapoptotic BCL-2 family member MCL-1, encodes a proapoptotic protein possessing only the BH3 domain [J].

Bae, J ;

Leo, CP ;

Hsu, SY ;

Hsueh, AJW .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (33) :25255-25261

[7] Alternative splicing and protein structure evolution [J].

Birzele, Fabian ;

Csaba, Gergely ;

Zimmer, Ralf .

NUCLEIC ACIDS RESEARCH, 2008, 36 (02) :550-558

[8] bcl-2 protein downregulation is not required for differentiation of multidrug resistant HL60 leukemia cells [J].

Blagosklonny, MV ;

Alvarez, M ;

Fojo, A ;

Neckers, LM .

LEUKEMIA RESEARCH, 1996, 20 (02) :101-107

[9] BCL2DB: moving 'helix-bundled' BCL-2 family members to their database [J].

Blaineau, Stanislas Valentin ;

Aouacheria, Abdel .

APOPTOSIS, 2009, 14 (07) :923-925

[10] Gene structure, alternative splicing, and chromosomal localization of pro-apoptotic Bcl-2 relative Bim [J].

Bouillet, P ;

Zhang, LC ;

Huang, DCS ;

Webb, GC ;

Bottema, CDK ;

Shore, P ;

Eyre, HJ ;

Sutherland, GR ;

Adams, JM .

MAMMALIAN GENOME, 2001, 12 (02) :163-168

← 1 2 3 4 5 6 7 8 9 10 →