Gelsolin superfamily proteins: key regulators of cellular functions

被引:328
作者
Silacci, P [1 ]
Mazzolai, L
Gauci, C
Stergiopulos, N
Yin, HL
Hayoz, D
机构
[1] Swiss Fed Inst Technol, Lab Hemodynaam & Cardiovasc Technol, CH-1015 Lausanne, Switzerland
[2] Univ Hosp, Serv Angiol, Lausanne, Switzerland
[3] Univ Texas, SW Med Ctr, Dept Physiol, Dallas, TX 75235 USA
关键词
gelsolin; gelsolin superfamily; cytoskeleton; apoptosis; phagocytosis; actin network;
D O I
10.1007/s00018-004-4225-6
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
Cytoskeletal rearrangement occurs in a variety of cellular processes and involves a wide spectrum of proteins. Among these, the gelsolin superfamily proteins control actin organization by severing filaments, capping filament ends and nucleating actin assembly [1]. Gelsolin is the founding member of this family, which now contains at least another six members: villin, adseverin, capG, advillin, supervillin and flightless I. In addition to their respective role in actin filament remodeling, these proteins have some specific and apparently non-overlapping particular roles in several cellular processes, including cell motility, control of apoptosis and regulation of phagocytosis (summarized in table 1). Evidence suggests that proteins belonging to the gelsolin superfamily may be involved in other processes, including gene expression regulation. This review will focus on some of the known functions of the gelsolin superfamily proteins, thus providing a basis for reflection on other possible and as yet incompletely understood roles for these proteins.
引用
收藏
页码:2614 / 2623
页数:10
相关论文
共 117 条
[61]   Developmentally essential protein flightless I is a nuclear receptor coactivator with actin binding activity [J].
Lee, YH ;
Campbell, HD ;
Stallcup, MR .
MOLECULAR AND CELLULAR BIOLOGY, 2004, 24 (05) :2103-2117
[62]   DIFFERENTIAL REGULATION OF INTEGRIN-MEDIATED PROPLATELET FORMATION AND MEGAKARYOCYTE SPREADING [J].
LEVEN, RM .
JOURNAL OF CELLULAR PHYSIOLOGY, 1995, 163 (03) :597-607
[63]   Molecular dynamics study of a gelsolin-derived peptide binding to a lipid bilayer containing phosphatidylinositol 4,5-bisphosphate [J].
Liepina, I ;
Czaplewski, C ;
Janmey, P ;
Liwo, A .
BIOPOLYMERS, 2003, 71 (01) :49-70
[64]   Delayed retraction of filopodia in gelsolin null mice [J].
Lu, M ;
Witke, W ;
Kwiatkowski, DJ ;
Kosik, KS .
JOURNAL OF CELL BIOLOGY, 1997, 138 (06) :1279-1287
[65]   Phosphoinositide 3-kinase in rat liver nuclei [J].
Lu, PJ ;
Hsu, AL ;
Wang, DS ;
Yan, HY ;
Yin, HL ;
Chen, CS .
BIOCHEMISTRY, 1998, 37 (16) :5738-5745
[66]   ORIGIN AND DEVELOPMENT OF DEMARCATION SYSTEM IN MEGAKARYOCYTES OF RAT BONE-MARROW [J].
MACPHERSON, GG .
JOURNAL OF ULTRASTRUCTURE RESEARCH, 1972, 40 (1-2) :167-+
[67]  
Marcu MG, 1996, BLOOD, V87, P20
[68]   ISOLATION AND CHARACTERIZATION OF CARDIAC AMYLOID IN FAMILIAL AMYLOID POLYNEUROPATHY TYPE-IV (FINNISH) - RELATION OF THE AMYLOID PROTEIN TO VARIANT GELSOLIN [J].
MAURY, CPJ .
BIOCHIMICA ET BIOPHYSICA ACTA, 1990, 1096 (01) :84-86
[69]   FINNISH HEREDITARY AMYLOIDOSIS IS CAUSED BY A SINGLE NUCLEOTIDE SUBSTITUTION IN THE GELSOLIN GENE [J].
MAURY, CPJ ;
KERE, J ;
TOLVANEN, R ;
DELACHAPELLE, A .
FEBS LETTERS, 1990, 276 (1-2) :75-77
[70]   FINNISH HEREDITARY AMYLOIDOSIS - AMINO-ACID-SEQUENCE HOMOLOGY BETWEEN THE AMYLOID FIBRIL PROTEIN AND HUMAN PLASMA GELSOLINE [J].
MAURY, CPJ ;
ALLI, K ;
BAUMANN, M .
FEBS LETTERS, 1990, 260 (01) :85-87