scholarly journals Characterization and sequence of the promoter region of the human epidermal growth factor receptor gene.

1985 ◽  
Vol 82 (15) ◽  
pp. 4920-4924 ◽  
Author(s):  
S. Ishii ◽  
Y. H. Xu ◽  
R. H. Stratton ◽  
B. A. Roe ◽  
G. T. Merlino ◽  
...  
1987 ◽  
Vol 7 (7) ◽  
pp. 2597-2601
Author(s):  
M Tal ◽  
C R King ◽  
M H Kraus ◽  
A Ullrich ◽  
J Schlessinger ◽  
...  

We localized the 5' region of the human gene HER2 in a cloned fragment of genomic DNA. This clone contained exons 1 to 4 of HER2, spanning the coding sequence for the first 191 amino acids. The promoter region of HER2 was identified upstream to exon 1 by nuclease S1 mapping and by a functional assay in which the promoter region drives the expression of a chloramphenicol acetyltransferase gene. The HER2 promoter is different from the promoter of the epidermal growth factor receptor gene (HER1), and the GC boxes which are typical of the promoter of the epidermal growth factor receptor gene are absent from the HER2 promoter. One major and two minor RNA start sites located at nucleotides 178, 244, and 257 upstream to the initiator ATG were identified. The first one is 21 and 70 base pairs downstream from typical TATAA and CAAT boxes, respectively. This indicates that transcription of HER2/neu can be regulated by a mechanism involving a TATA box, as well as by other unidentified regulatory elements.


1993 ◽  
Vol 292 (2) ◽  
pp. 591-595
Author(s):  
A del Arco ◽  
M Izquierdo

A novel restriction polymorphism, probably due to tissue-specific methylation, has been identified at the human epidermal-growth-factor-receptor (EGF-R) gene. DNA isolated from smooth muscle showed altered EcoRI restriction bands when hybridized with different fragments of the EGF-R cDNA. These bands were absent in brain or leucocyte DNA samples from the same individuals. Three restriction sites, partly resistant to cleavage by EcoRI, were characterized in muscle DNA which were not clustered but instead were scattered along the gene. The flanking sequences of one of these resistant EcoRI sites were determined. This specific EcoRI site was followed by a 3′-guanosine generating a methylatable EcoRI sequence. This suggests that the failure to digest to completion these EcoRI sites was due to modification by methylation. In addition, we noted that EcoRI sites were affected at both alleles, indicating that de novo methylation changes, and not methylation events related to genomic imprinting, would cause the muscle-specific EcoRI pattern. Also abnormal restriction fragments with XbaI were observed in muscle DNA. A large number of unrelated muscle DNA samples have been analysed, and all of them displayed an identical EcoRI polymorphic pattern, suggesting that DNA modification by de novo methylation events could be functionally relevant.


Oncogene ◽  
1997 ◽  
Vol 15 (9) ◽  
pp. 1095-1101 ◽  
Author(s):  
M Saeed Sheikh ◽  
France Carrier ◽  
Alfred C Johnson ◽  
Sara E Ogdon ◽  
Albert J Fornace Jr

1987 ◽  
Vol 7 (7) ◽  
pp. 2597-2601 ◽  
Author(s):  
M Tal ◽  
C R King ◽  
M H Kraus ◽  
A Ullrich ◽  
J Schlessinger ◽  
...  

We localized the 5' region of the human gene HER2 in a cloned fragment of genomic DNA. This clone contained exons 1 to 4 of HER2, spanning the coding sequence for the first 191 amino acids. The promoter region of HER2 was identified upstream to exon 1 by nuclease S1 mapping and by a functional assay in which the promoter region drives the expression of a chloramphenicol acetyltransferase gene. The HER2 promoter is different from the promoter of the epidermal growth factor receptor gene (HER1), and the GC boxes which are typical of the promoter of the epidermal growth factor receptor gene are absent from the HER2 promoter. One major and two minor RNA start sites located at nucleotides 178, 244, and 257 upstream to the initiator ATG were identified. The first one is 21 and 70 base pairs downstream from typical TATAA and CAAT boxes, respectively. This indicates that transcription of HER2/neu can be regulated by a mechanism involving a TATA box, as well as by other unidentified regulatory elements.


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