Status of p53 in first-trimester cytotrophoblastic cells

被引:14
作者
Cohen, M. [1 ]
Meisser, A. [1 ]
Haenggeli, L. [1 ]
Irminger-Finger, I. [1 ]
Bischof, P. [1 ]
机构
[1] Univ Geneva, Lab Hormonol, Dept Obstet & Gynaecol, CH-1211 Geneva 14, Switzerland
关键词
complex; CTB; cytoplasm; nucleus; p53;
D O I
10.1093/molehr/gal105
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
p53 has been called the cellular gatekeeper of the genome because it can induce cell-cycle arrest in G1, apoptosis or affect DNA replication in response to DNA damage. As p53 has been observed in first-trimester cytotrophoblastic cells (CTB), but its expression in normal cells is generally not detectable because of its short half-life, p53 could play an important role in cellular differentiation and/or in the control of the invasion of trophoblastic cells; therefore, p53 status was investigated in these cells. Using different antibodies recognizing different epitopes of p53 protein, abundant p53 expression was observed both in nuclear and in cytoplasmic compartments of first-trimester CTB. Whereas p53 was detected in the nuclei of few trophoblastic cells with an antibody recognizing the N-terminal epitope of the protein, high expression level of p53 in the cytoplasm of CTB was detected with an antibody recognizing the middle part of p53. The lack of immunoreactivity of p53 with antibodies recognizing the epitopes located at the N-terminus of p53 and the high level of p53 protein observed in the cytoplasm of CTB suggest that the N-terminus of p53 is involved in the formation of complexes. These cytoplasmic complexes were detected under non-reducing conditions in western blot analysis and had apparent molecular weights (MW) of 195, 167 or 125 kDa. These complexes could prolong the half-life of p53 in the cytoplasm of CTBs. By contrast, in the nuclei of CTBs, p53 seems to be present as a tetramer.
引用
收藏
页码:111 / 116
页数:6
相关论文
共 30 条
[1]   ES cells do not activate p53-dependent stress responses and undergo p53-independent apoptosis in response to DNA damage [J].
Aladjem, MI ;
Spike, BT ;
Rodewald, LW ;
Hope, TJ ;
Klemm, M ;
Jaenisch, R ;
Wahl, GM .
CURRENT BIOLOGY, 1998, 8 (03) :145-155
[2]  
ALMOG N, 1997, BIOCHIM BIOPHYS ACTA, V1333, P1
[3]   Transcriptional activation by p53 of the human type IV collagenase (gelatinase A or matrix metalloproteinase 2) promoter [J].
Bian, JH ;
Sun, Y .
MOLECULAR AND CELLULAR BIOLOGY, 1997, 17 (11) :6330-6338
[4]  
Bischof P, 1995, Early Pregnancy, V1, P263
[5]  
Bonsing BA, 1997, CYTOMETRY, V28, P11, DOI 10.1002/(SICI)1097-0320(19970501)28:1<11::AID-CYTO2>3.3.CO
[6]  
2-H
[7]   p53 isoforms can regulate p53 transcriptional activity [J].
Bourdon, JC ;
Fernandes, K ;
Murray-Zmijewski, F ;
Liu, G ;
Diot, A ;
Xirodimas, DP ;
Saville, MK ;
Lane, DP .
GENES & DEVELOPMENT, 2005, 19 (18) :2122-2137
[8]   Metalloproteinases and human placental invasiveness [J].
Cohen, M. ;
Meisser, A. ;
Bischof, P. .
PLACENTA, 2006, 27 (08) :783-793
[9]   ΔN-p53, a natural isoform of p53 lacking the first transactivation domain, counteracts growth suppression by wild-type p53 [J].
Courtois, S ;
Verhaegh, G ;
North, S ;
Luciani, MG ;
Lassus, P ;
Hibner, U ;
Oren, M ;
Hainaut, P .
ONCOGENE, 2002, 21 (44) :6722-6728
[10]   p53 protein variants: structural and functional similarities with p63 and p73 isoforms [J].
Courtois, S ;
de Fromentel, CC ;
Hainaut, P .
ONCOGENE, 2004, 23 (03) :631-638