A canonical nerve growth factor-induced gene-B response element appears not to be involved in the cyclic adenosine monophosphate-dependent expression of differentiation in thyrocytes

被引:5
作者
Pichon, B
Vassart, G
Christophe, D
机构
[1] ULB, Fac Med, IRIBHN, B-1070 Brussels, Belgium
[2] Hop Erasme, Serv Genet Med, B-1070 Brussels, Belgium
关键词
cAMP; NGFI-B; thyroid; transcription;
D O I
10.1016/S0303-7207(99)00104-5
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The expression of transcriptionally active nerve growth factor-induced gene-B (NGFI-B) is rapidly induced in thyroid follicular cells in response to cAMP stimulation. As the transcription of thyrocyte-specific genes is controlled by the cAMP cascade, we have investigated a possible involvement of NGFI-B in this control. Recombinant adenoviruses driving the expression of either the intact NGFI-B protein or a truncated form of it that lacks the capacity to transactivate a NBRE-dependent promoter, were used to infect dog thyrocytes maintained in primary culture. Northern blot analysis of total RNA from infected cells revealed that the expression of NGFI-B was not sufficient to induce a significant accumulation of specific transcripts (thyroglobulin, thyroperoxidase, sodium-iodide symporter) in unstimulated thyrocytes. The overproduction of the transcriptionally inactive form of NGFI-B in thyrocytes maintained in the presence of forskolin after infection did not impair the accumulation of the thyroid-specific transcripts. These data show that NGFI-B does not control the expression of differentiation in thyrocytes by acting through a canonical NBRE. As a consequence, we must consider that either the expression of NGFI-B in cAMP-stimulated thyrocytes is not critically linked to the expression of differentiation or that NGFI-B is implicated in a regulatory mechanism which differs from its known action at the level of a NBRE. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:21 / 27
页数:7
相关论文
共 23 条
[1]  
[Anonymous], 1988, Antibodies: A Laboratory Manual
[2]   INDUCTION OF C-FOS AND TIS GENES IN CULTURED RAT ASTROCYTES BY NEUROTRANSMITTERS [J].
ARENANDER, AT ;
DEVELLIS, J ;
HERSCHMAN, HR .
JOURNAL OF NEUROSCIENCE RESEARCH, 1989, 24 (01) :107-114
[3]   REPORTER CONSTRUCTS WITH LOW BACKGROUND ACTIVITY UTILIZING THE CAT GENE [J].
BOSHART, M ;
KLUPPEL, M ;
SCHMIDT, A ;
SCHUTZ, G ;
LUCKOW, B .
GENE, 1992, 110 (01) :129-130
[4]   Expression of a transactivation-deficient form of thyroid transcription factor I decreases the activity of co-transfected thyroglobulin and thyroperoxidase promoters [J].
ChristopheHobertus, C ;
vanRenterghem, P ;
Pichon, B ;
Christophe, D .
FEBS LETTERS, 1996, 399 (1-2) :140-142
[5]  
CRAWFORD PA, 1995, MOL CELL BIOL, V15, P4331
[6]   Cloning and characterization of the thyroid iodide transporter [J].
Dai, G ;
Levy, O ;
Carrasco, N .
NATURE, 1996, 379 (6564) :458-460
[7]   FUNCTIONAL DOMAINS AND PHOSPHORYLATION OF THE ORPHAN RECEPTOR NUR77 [J].
DAVIS, IJ ;
HAZEL, TG ;
CHEN, RH ;
BLENIS, J ;
LAU, LF .
MOLECULAR ENDOCRINOLOGY, 1993, 7 (08) :953-964
[8]   TRANSCRIPTIONAL ACTIVATION BY NUR77, A GROWTH FACTOR-INDUCIBLE MEMBER OF THE STEROID-HORMONE RECEPTOR SUPERFAMILY [J].
DAVIS, IJ ;
HAZEL, TG ;
LAU, LF .
MOLECULAR ENDOCRINOLOGY, 1991, 5 (06) :854-859
[9]   UNIQUE RESPONSE PATHWAYS ARE ESTABLISHED BY ALLOSTERIC INTERACTIONS AMONG NUCLEAR HORMONE RECEPTORS [J].
FORMAN, BM ;
UMESONO, K ;
CHEN, J ;
EVANS, RM .
CELL, 1995, 81 (04) :541-550
[10]  
GOMEZFOIX AM, 1992, J BIOL CHEM, V267, P25129