Computer modeling of promoter organization as a tool to study transcriptional coregulation

被引:65
作者
Werner, T
Fessele, S
Maier, H
Nelson, PJ
机构
[1] Univ Munich, Med Poliklin, D-80336 Munich, Germany
[2] GSF, Natl Res Ctr Environm & Hlth, Inst Expt Genet, Neuherberg, Germany
[3] Genomatix Software GmbH, D-80339 Munich, Germany
关键词
promoter; modeling; bioinformatics; module; functional context;
D O I
10.1096/fj.02-0955rev
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
Understanding how the regulation of gene networks is orchestrated is an important challenge for characterizing complex biological processes. Gene transcription is regulated in part by nuclear factors that recognize short DNA sequence motifs, called transcription factor binding sites, in most cases located upstream of the gene coding sequence in promoter and enhancer regions. Genes expressed in the same tissue under similar conditions often share a common organization of at least some of these regulatory binding elements. In this way the organization of promoter motifs represents a "footprint" of the transcriptional regulatory mechanisms at work in a specific biologic context and thus provides information about signal and tissue specific control of expression. Analysis of promoters for organizational features as demonstrated here provides a crucial link between the static nucleotide sequence of the genome and the dynamic aspects of gene regulation and expression.
引用
收藏
页码:1228 / 1237
页数:10
相关论文
共 63 条
[21]   CLONING AND DIFFERENTIAL TISSUE-SPECIFIC EXPRESSION OF 3 MOUSE BETA-CHEMOKINE RECEPTOR-LIKE GENES, INCLUDING THE GENE FOR A FUNCTIONAL MACROPHAGE INFLAMMATORY PROTEIN-1-ALPHA RECEPTOR [J].
GAO, JL ;
MURPHY, PM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (29) :17494-17501
[22]   Impaired host defense, hematopoiesis, guanulomatous inflammation and type 1-type 2 cytokine balance in mice lacking CC chemokine receptor 1 [J].
Gao, JL ;
Wynn, TA ;
Chang, Y ;
Lee, EJ ;
Broxmeyer, HE ;
Cooper, S ;
Tiffany, HL ;
Westphal, H ;
KwonChung, J ;
Murphy, PM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 185 (11) :1959-1968
[23]   Urokinase is required for T lymphocyte proliferation and activation in vitro [J].
Gyetko, MR ;
Libre, EA ;
Fuller, JA ;
Chen, GH ;
Toews, GB .
JOURNAL OF LABORATORY AND CLINICAL MEDICINE, 1999, 133 (03) :274-288
[24]   Expanding the TRANSFAC database towards an expert system of regulatory molecular mechanisms [J].
Heinemeyer, T ;
Chen, X ;
Karas, H ;
Kel, AE ;
Kel, OV ;
Liebich, I ;
Meinhardt, T ;
Reuter, I ;
Schacherer, F ;
Wingender, E .
NUCLEIC ACIDS RESEARCH, 1999, 27 (01) :318-322
[25]   CD26/dipeptidyl peptidase IV differentially regulates the chemotaxis of T cells and monocytes toward RANTES: possible mechanism for the switch from innate to acquired immune response [J].
Iwata, S ;
Yamaguchi, N ;
Munakata, Y ;
Ikushima, H ;
Lee, JF ;
Hosono, O ;
Schlossman, SF ;
Morimoto, C .
INTERNATIONAL IMMUNOLOGY, 1999, 11 (03) :417-426
[26]  
Kel A E, 1995, Proc Int Conf Intell Syst Mol Biol, V3, P197
[27]   Plasma lipoproteins promote the release of bacterial lipopolysaccharide from the monocyte cell surface [J].
Kitchens, RL ;
Wolfbauer, G ;
Albers, JJ ;
Munford, RS .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (48) :34116-34122
[28]   Functional promoter modules can be defected by formal models independent of overall nucleoside sequence similarity [J].
Klingenhoff, A ;
Frech, K ;
Quandt, K ;
Werner, T .
BIOINFORMATICS, 1999, 15 (03) :180-186
[29]  
Klingenhoff A., 2002, In Silico Biology, V2, pS17
[30]   Endothelial cells at inflammatory sites as target for therapeutic intervention [J].
Koning, GA ;
Schiffelers, RM ;
Storm, G .
ENDOTHELIUM-JOURNAL OF ENDOTHELIAL CELL RESEARCH, 2002, 9 (03) :161-171