TRANSCRIPTIONAL CONTROL OF PANCREATIC-ISLET HORMONES GENE-EXPRESSION

被引:9
作者
KNEPEL, W
机构
[1] Department of Biochemical Pharmacology, University of Goettingen/Germany
来源
EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY | 1993年 / 101卷 / 01期
关键词
PANCREATIC ISLET HORMONES; TRANSCRIPTIONAL CONTROL; GENE EXPRESSION;
D O I
10.1055/s-0029-1211206
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Initiation of transcription requires transcription factors that recognize specific DNA sequences present in promoters and enhancers of the respective genes. Cell-specific expression of the pancreatic islet hormone genes is conferred by a cell-specific combination of transcription factors. The DNA binding sites and cDNAs of some of them have been characterized. An islet-specific enhancer-binding protein of the rat glucagon gene recognizes also cis-acting elements of the rat insulin I and rat somatostatin genes. Thus identical or related factors may be involved in the expression of these pancreatic genes, reflecting that the different islet cell types arise from a common progenitor cell. The characterization of islet-specific transcription factors may lead to regulatory genes whose products specify islet cell phenotypes during development. Basal transcriptional activity of islet hormone genes can be enhanced by metabolic, humoral or nerval signals via various second messenger systems. Cyclic AMP acts through distinct response elements. The islet cells are electrically excitable and known secretagogues increase electrical activity and elevate cytosolic calcium concentration. Depolarization-induced activation of voltage-dependent calcium channels stimulates rat glucagon gene transcription suggesting that calcium is an intracellular signal for pancreatic islet hormone gene transcription.
引用
收藏
页码:39 / 45
页数:7
相关论文
共 39 条
[21]   PAN - A TRANSCRIPTIONAL REGULATOR THAT BINDS CHYMOTRYPSIN, INSULIN, AND AP-4 ENHANCER MOTIFS [J].
NELSON, C ;
SHEN, LP ;
MEISTER, A ;
FODOR, E ;
RUTTER, WJ .
GENES & DEVELOPMENT, 1990, 4 (06) :1035-1043
[22]   THE STEROID-RECEPTOR SUPERFAMILY - MORE EXCITEMENT PREDICTED FOR THE FUTURE [J].
OMALLEY, B .
MOLECULAR ENDOCRINOLOGY, 1990, 4 (03) :363-369
[23]   AN INVIVO ANALYSIS OF PANCREATIC PROTEIN AND INSULIN-BIOSYNTHESIS IN A RAT MODEL FOR NON-INSULIN-DEPENDENT DIABETES [J].
PERMUTT, MA ;
KAKITA, K ;
MALINAS, P ;
KARL, I ;
BONNERWEIR, S ;
WEIR, G ;
GIDDINGS, SJ .
JOURNAL OF CLINICAL INVESTIGATION, 1984, 73 (05) :1344-1350
[24]   GENETICS OF NIDDM [J].
PERMUTT, MA .
DIABETES CARE, 1990, 13 (11) :1150-1153
[25]   ALPHA-CELL-SPECIFIC EXPRESSION OF THE GLUCAGON GENE IS CONFERRED TO THE GLUCAGON PROMOTER ELEMENT BY THE INTERACTIONS OF DNA-BINDING PROTEINS [J].
PHILIPPE, J ;
DRUCKER, DJ ;
KNEPEL, W ;
JEPEAL, L ;
MISULOVIN, Z ;
HABENER, JF .
MOLECULAR AND CELLULAR BIOLOGY, 1988, 8 (11) :4877-4888
[26]  
PHILIPPE J, 1990, J BIOL CHEM, V265, P1465
[27]   INSULIN PRODUCTION AND GLUCOSE-METABOLISM IN ISOLATED PANCREATIC-ISLETS OF RATS WITH NIDDM [J].
PORTHA, B ;
GIROIX, MH ;
SERRADAS, P ;
WELSH, N ;
HELLERSTROM, C ;
SENER, A ;
MALAISSE, WJ .
DIABETES, 1988, 37 (09) :1226-1233
[28]  
POWERS AC, 1989, J BIOL CHEM, V264, P10048
[29]   MAPPING GENES IN DIABETES - GENETIC EPIDEMIOLOGIC PERSPECTIVE [J].
RICH, SS .
DIABETES, 1990, 39 (11) :1315-1319
[30]   GENE-REGULATION - MORE TO MUSCLE THAN MYOD [J].
ROBERTSON, M .
NATURE, 1990, 344 (6265) :378-379