JEM-1, a novel gene encoding a leucine-zipper nuclear factor upregulated during retinoid-induced maturation of NB4 promyelocytic leukaemia

被引:24
作者
Duprez, E
Tong, JH
Derre, J
Chen, SJ
Berger, R
Chen, Z
Lanotte, M
机构
[1] HOP ST LOUIS,INSERM U301,CTR G HAYEM,F-75475 PARIS,FRANCE
[2] RUI JIN HOSP,INST HEMATOL,SHANGHAI,PEOPLES R CHINA
基金
中国国家自然科学基金;
关键词
leukaemia; differentiation; retinoids; nuclear factors; cloning;
D O I
10.1038/sj.onc.1200995
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
Retinoid-induced proliferation causing hyperleukocytosis is a severe complication of retinoid therapy in t(15;17) acute promyelocytic leukaemia. The molecular basis of this phenomenon is unknown. It is possible that the transiently enhanced cell proliferation results from RA-induction of growth regulatory genes. Using Differential Display of cDNAs from NB4 cells we have identified Jem, a novel gene transcript which is upregulated by retinoids during the early proliferative response in maturating cells but not in resistant cells. A 2.7 kb cDNA was cloned and sequenced. The open reading frame contains a 400 amino acid sequence corresponding to a novel 45 kDa basic protein (pI 8.9). The JEM DNA sequence is detected by FISH on human chromosome 1 at q24. The Jem peptide sequence shows a 'leucine-zipper' dimerisation motif with limited homology to Fos/Jun and ATF/CREB proteins and several putative phosphorylation sites. An atypical basic region may correspond to an unknown DNA-binding domain. The C-terminal end of Jem spans a long stretch featuring a PEST motif. After transfection into COS cells, the Jem protein shows a ponctuated nuclear localisation. We hypothesise that this novel nuclear factor may act as a transcription factor, or coregulator, involved in either cell growth control and/or maturation.
引用
收藏
页码:1563 / 1570
页数:8
相关论文
共 35 条
[1]   MOLECULAR ANALYSIS OF ACUTE PROMYELOCYTIC LEUKEMIA BREAKPOINT CLUSTER REGION ON CHROMOSOME-17 [J].
BORROW, J ;
GODDARD, AD ;
SHEER, D ;
SOLOMON, E .
SCIENCE, 1990, 249 (4976) :1577-1580
[2]   DIMERS, LEUCINE ZIPPERS AND DNA-BINDING DOMAINS [J].
BUSCH, SJ ;
SASSONECORSI, P .
TRENDS IN GENETICS, 1990, 6 (02) :36-40
[3]  
CASTAIGNE S, 1990, BLOOD, V76, P1704
[4]   RAR-SPECIFIC AGONIST/ANTAGONISTS WHICH DISSOCIATE TRANSACTIVATION AND AP1 TRANSREPRESSION INHIBIT ANCHORAGE-INDEPENDENT CELL-PROLIFERATION [J].
CHEN, JY ;
PENCO, S ;
OSTROWSKI, J ;
BALAGUER, P ;
PONS, M ;
STARRETT, JE ;
RECZEK, P ;
CHAMBON, P ;
GRONEMEYER, H .
EMBO JOURNAL, 1995, 14 (06) :1187-1197
[5]   SIMULTANEOUS LOCALIZATION OF COSMIDS AND CHROMOSOME R-BANDING BY FLUORESCENCE MICROSCOPY - APPLICATION TO REGIONAL MAPPING OF HUMAN CHROMOSOME-11 [J].
CHERIF, D ;
JULIER, C ;
DELATTRE, O ;
DERRE, J ;
LATHROP, GM ;
BERGER, R .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (17) :6639-6643
[6]   SINGLE-STEP METHOD OF RNA ISOLATION BY ACID GUANIDINIUM THIOCYANATE PHENOL CHLOROFORM EXTRACTION [J].
CHOMCZYNSKI, P ;
SACCHI, N .
ANALYTICAL BIOCHEMISTRY, 1987, 162 (01) :156-159
[7]   THE UBIQUITIN-PROTEASOME PROTEOLYTIC PATHWAY [J].
CIECHANOVER, A .
CELL, 1994, 79 (01) :13-21
[8]   THE T(15-17) TRANSLOCATION OF ACUTE PROMYELOCYTIC LEUKEMIA FUSES THE RETINOIC ACID RECEPTOR-ALPHA GENE TO A NOVEL TRANSCRIBED LOCUS [J].
DETHE, H ;
CHOMIENNE, C ;
LANOTTE, M ;
DEGOS, L ;
DEJEAN, A .
NATURE, 1990, 347 (6293) :558-561
[9]  
DIGNAM JDL, 1983, NUCLEIC ACIDS RES, V11, P1495
[10]   THE PML RETINOIC ACID RECEPTOR-ALPHA TRANSLOCATION CONVERTS THE RECEPTOR FROM AN INHIBITOR TO A RETINOIC ACID-DEPENDENT ACTIVATOR OF TRANSCRIPTION FACTOR-AP-1 [J].
DOUCAS, V ;
BROCKES, JP ;
YANIV, M ;
DETHE, H ;
DEJEAN, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (20) :9345-9349