scholarly journals Human cysteine dioxygenase type I (CDO-I; EC 1.13.11.20): 5' flanking region and intron-exon structure of the gene.

1997 ◽  
Vol 50 (5) ◽  
pp. 269-271 ◽  
Author(s):  
D B Ramsden ◽  
A Kapadi ◽  
N J Fitch ◽  
M J Farmer ◽  
P Bennett ◽  
...  
Keyword(s):  
Type I ◽  
Cysteine Dioxygenase ◽  
Flanking Region ◽  
Exon Structure

Regulatory elements in the 5'-flanking region and the first intron contribute to transcriptional control of the mouse alpha 1 type I collagen gene

1989 ◽  
Vol 9 (5) ◽  
pp. 2224-2227
Author(s):  
R A Rippe ◽  
S I Lorenzen ◽  
D A Brenner ◽  
M Breindl
Keyword(s):  
Transcriptional Control ◽  
Type I Collagen ◽  
Regulatory Elements ◽  
Regulatory Sequences ◽  
Type I ◽  
Col1a1 Gene ◽  
First Intron ◽  
Flanking Region ◽  
Specific Regulation ◽  
High Level

We have identified two blocks of regulatory sequences located in the 5'-flanking region and the first intron of the mouse alpha 1 type I collagen (COL1A1) gene. Both blocks were found to contain positive as well as negative regulatory elements. Sequences located within 222 base pairs upstream of the transcription start site showed a strong stimulatory effect on the COL1A1 promoter and were sufficient for tissue-specific regulation of the COL1A1 gene. The combined upstream and intron regulatory sequences showed a marked inhibition of COL1A1 promoter activity in fibroblasts. This finding suggests that additional, more remote regulatory sequences may be required for establishing the high level of activity of the endogenous COL1A1 gene in fibroblastoid cells.

Regulation of collagen I gene expression by ras

1992 ◽  
Vol 12 (10) ◽  
pp. 4714-4723
Author(s):  
J L Slack ◽  
M I Parker ◽  
V R Robinson ◽  
P Bornstein
Keyword(s):  
Type I Collagen ◽  
The Body ◽  
Transformed Cells ◽  
Type I ◽  
Mrna Levels ◽  
Oncogenic Ras ◽  
Genes Encoding ◽  
Flanking Region ◽  
Collagen Genes ◽  
I Gene

Although transformation of rodent fibroblasts can lead to dramatic changes in expression of extracellular matrix genes, the molecular basis and physiological significance of these changes remain poorly understood. In this study, we have investigated the mechanism(s) by which ras affects expression of the genes encoding type I collagen. Levels of both alpha 1(I) and alpha 2(I) collagen mRNAs were markedly reduced in Rat 1 fibroblasts overexpressing either the N-rasLys-61 or the Ha-rasVal-12 oncogene. In fibroblasts conditionally transformed with N-rasLys-61, alpha 1(I) transcript levels began to decline within 8 h of ras induction and reached 1 to 5% of control levels after 96 h. In contrast, overexpression of normal ras p21 had no effect on alpha 1(I) or alpha 2(I) mRNA levels. Nuclear run-on experiments demonstrated that the transcription rates of both the alpha 1(I) and alpha 2(I) genes were significantly reduced in ras-transformed cells compared with those in parental cells. In addition, the alpha 1(I) transcript was less stable in transformed cells. Chimeric plasmids containing up to 3.6 kb of alpha 1(I) 5'-flanking DNA and up to 2.3 kb of the 3'-flanking region were expressed at equivalent levels in both normal and ras-transformed fibroblasts. However, a cosmid clone containing the entire mouse alpha 1(I) gene, including 3.7 kb of 5'- and 4 kb of 3'-flanking DNA, was expressed at reduced levels in fibroblasts overexpressing oncogenic ras. We conclude that oncogenic ras regulates the type I collagen genes at both transcriptional and posttranscriptional levels and that this effect, at least for the alpha 1(I) gene, may be mediated by sequences located either within the body of the gene itself or in the distal 3'-flanking region.

scholarly journals Regulation of collagen I gene expression by ras.

1992 ◽  
Vol 12 (10) ◽  
pp. 4714-4723 ◽  
Author(s):  
J L Slack ◽  
M I Parker ◽  
V R Robinson ◽  
P Bornstein
Keyword(s):  
Type I Collagen ◽  
The Body ◽  
Transformed Cells ◽  
Type I ◽  
Mrna Levels ◽  
Oncogenic Ras ◽  
Genes Encoding ◽  
Flanking Region ◽  
Collagen Genes ◽  
I Gene

Although transformation of rodent fibroblasts can lead to dramatic changes in expression of extracellular matrix genes, the molecular basis and physiological significance of these changes remain poorly understood. In this study, we have investigated the mechanism(s) by which ras affects expression of the genes encoding type I collagen. Levels of both alpha 1(I) and alpha 2(I) collagen mRNAs were markedly reduced in Rat 1 fibroblasts overexpressing either the N-rasLys-61 or the Ha-rasVal-12 oncogene. In fibroblasts conditionally transformed with N-rasLys-61, alpha 1(I) transcript levels began to decline within 8 h of ras induction and reached 1 to 5% of control levels after 96 h. In contrast, overexpression of normal ras p21 had no effect on alpha 1(I) or alpha 2(I) mRNA levels. Nuclear run-on experiments demonstrated that the transcription rates of both the alpha 1(I) and alpha 2(I) genes were significantly reduced in ras-transformed cells compared with those in parental cells. In addition, the alpha 1(I) transcript was less stable in transformed cells. Chimeric plasmids containing up to 3.6 kb of alpha 1(I) 5'-flanking DNA and up to 2.3 kb of the 3'-flanking region were expressed at equivalent levels in both normal and ras-transformed fibroblasts. However, a cosmid clone containing the entire mouse alpha 1(I) gene, including 3.7 kb of 5'- and 4 kb of 3'-flanking DNA, was expressed at reduced levels in fibroblasts overexpressing oncogenic ras. We conclude that oncogenic ras regulates the type I collagen genes at both transcriptional and posttranscriptional levels and that this effect, at least for the alpha 1(I) gene, may be mediated by sequences located either within the body of the gene itself or in the distal 3'-flanking region.

scholarly journals Polymorphism of the 5′‐Flanking Region of the Tumor Necrosis Factor (TNF)–α Gene and Susceptibility to Human T‐Cell Lymphotropic Virus Type I (HTLV‐I) Uveitis

1999 ◽  
Vol 180 (3) ◽  
pp. 880-883 ◽  
Author(s):  
Naoko Seki ◽  
Kazunari Yamaguchi ◽  
Akira Yamada ◽  
Shintaro Kamizono ◽  
Sunao Sugita ◽  
...  
Keyword(s):  
T Cell ◽  
Tumor Necrosis Factor ◽  
Virus Type ◽  
Tumor Necrosis ◽  
Type I ◽  
Human T Cell ◽  
Tnf Α ◽  
Flanking Region ◽  
Necrosis Factor

Human cysteine dioxygenase type I: primary structure derived from base sequencing of cDNA

1994 ◽  
Vol 1209 (1) ◽  
pp. 107-110 ◽  
Author(s):  
Karen P. McCann ◽  
Mohammed T. Akbari ◽  
Adrian C. Williams ◽  
David B. Ramsden
Keyword(s):  
Primary Structure ◽  
Type I ◽  
Cysteine Dioxygenase ◽  
Base Sequencing

scholarly journals Regulatory elements in the 5'-flanking region and the first intron contribute to transcriptional control of the mouse alpha 1 type I collagen gene.

1989 ◽  
Vol 9 (5) ◽  
pp. 2224-2227 ◽  
Author(s):  
R A Rippe ◽  
S I Lorenzen ◽  
D A Brenner ◽  
M Breindl
Keyword(s):  
Transcriptional Control ◽  
Type I Collagen ◽  
Regulatory Elements ◽  
Regulatory Sequences ◽  
Type I ◽  
Col1a1 Gene ◽  
First Intron ◽  
Flanking Region ◽  
Specific Regulation ◽  
High Level

We have identified two blocks of regulatory sequences located in the 5'-flanking region and the first intron of the mouse alpha 1 type I collagen (COL1A1) gene. Both blocks were found to contain positive as well as negative regulatory elements. Sequences located within 222 base pairs upstream of the transcription start site showed a strong stimulatory effect on the COL1A1 promoter and were sufficient for tissue-specific regulation of the COL1A1 gene. The combined upstream and intron regulatory sequences showed a marked inhibition of COL1A1 promoter activity in fibroblasts. This finding suggests that additional, more remote regulatory sequences may be required for establishing the high level of activity of the endogenous COL1A1 gene in fibroblastoid cells.

scholarly journals Inhibition of MuSK Expression by CREB Interacting with a CRE-Like Element and MyoD

2005 ◽  
Vol 25 (13) ◽  
pp. 5329-5338 ◽  
Author(s):  
Chang-Hoon Kim ◽  
Wen C. Xiong ◽  
Lin Mei
Keyword(s):  
Promoter Activity ◽  
Protein Tyrosine Kinase ◽  
Type I ◽  
Inhibitory Mechanism ◽  
Junction Formation ◽  
Cyclic Amp Response Element ◽  
Myogenic Factor ◽  
Flanking Region ◽  
Underlying Mechanisms ◽  
Interfering Rna

ABSTRACT The type I receptor-like protein tyrosine kinase MuSK is essential for the neuromuscular junction formation. MuSK expression is tightly regulated during development, but the underlying mechanisms were unclear. Here we identified a novel mechanism by which MuSK expression may be regulated. A cyclic AMP response element (CRE)-like element in the 5′-flanking region of the MuSK gene binds to CREB1 (CRE-binding protein 1). Mutation of this element increases the MuSK promoter activity, suggesting a role for CREB1 in attenuation of MuSK expression. Interestingly, CREB mutants unable to bind to DNA also inhibit MuSK promoter activity, suggesting a CRE-independent inhibitory mechanism. In agreement, CREB1 could inhibit a mutant MuSK transgene reporter whose CRE site was mutated. We provide evidence that CREB interacts directly with MyoD, a myogenic factor essential for MuSK expression in muscle cells. Suppression of CREB expression by small interfering RNA increases MuSK promoter activity. These results demonstrate an important role for CREB1 in the regulation of MuSK expression.

scholarly journals Structure of the human hexokinase type I gene and nucleotide sequence of the 5′ flanking region

1998 ◽  
Vol 331 (2) ◽  
pp. 607-613 ◽  
Author(s):  
Annamaria RUZZO ◽  
Francesca ANDREONI ◽  
Mauro MAGNANI
Keyword(s):  
Yeast Artificial Chromosome ◽  
Direct Sequencing ◽  
Artificial Chromosome ◽  
Type I ◽  
Coding Region ◽  
Exon 1 ◽  
Flanking Region ◽  
The Individual ◽  
I Gene ◽  
Hexokinase Type I

This study reports the precise intron/exon boundaries and intron/exon composition of the human hexokinase type I gene. A yeast artificial chromosome containing the hexokinase type I gene was isolated from the yeast artificial chromosome library of the Centre d'Étude du Polymorphisme Humaine. A cosmid sublibrary was created and direct sequencing of the individual cosmids was used to provide the exon/intron organization. The human hexokinase type I gene was found to be composed of 18 exons ranging in size from 63 to 305 bp. Intron 1 is at least 15 kb in length, whereas intron 2 spans at least 10 kb. Overall, the length of the 17 introns ranges from 104 to greater than 15 kb. The entire coding region is contained in at least 75 kb of the gene. The structure of the gene reveals a remarkable conservation of the size of the exons compared with glucokinase and hexokinase type II. Isolation of the 5´ flanking region of the gene revealed a 75–90% identity with the rat sequence. Direct evidence of an alternative red-blood-cell-specific exon 1 located upstream of the 5´ flanking region of the gene is also provided.

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