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Unique expression of the human Evi-1 gene in an endometrial carcinoma cell line: sequence of cDNAs and structure of alternatively spliced transcripts.

Unique expression of the human Evi-1 gene in an endometrial carcinoma cell line: sequence of... Retroviral insertional activation of the expression of the Evi-1 is one of the most common events associated with transformation in murine myeloid leukemia. The murine Evi-1 gene encodes a 145 kDa nuclear, DNA binding protein that contains two domains containing seven and three sets of repeats of the zinc finger motif. During studies to determine the role of the Evi-1 gene in the transformation of human cells, we have found that the Evi-1 gene is uniquely expressed at low levels in HEC-1-A cells and at high levels in HEC-1-B cells, two related human endometrial carcinoma cell lines. cDNA clones were isolated and sequenced from the HEC-1-B cell line. The human gene is highly homologous to the murine gene and shows 91% and 94% homology in nucleotide or amino acid sequence respectively. In addition an alternatively spliced form of the gene was identified that encodes a protein with an internal deletion 315 amino acids including two of the zinc finger repeats. The possible basis for the unique expression of the Evi-1 gene by HEC-1 cells could not be determined by karyotype or Southern blot analysis. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Oncogene Pubmed

Unique expression of the human Evi-1 gene in an endometrial carcinoma cell line: sequence of cDNAs and structure of alternatively spliced transcripts.

Oncogene , Volume 5 (7): 9 – Aug 30, 1990

Unique expression of the human Evi-1 gene in an endometrial carcinoma cell line: sequence of cDNAs and structure of alternatively spliced transcripts.


Abstract

Retroviral insertional activation of the expression of the Evi-1 is one of the most common events associated with transformation in murine myeloid leukemia. The murine Evi-1 gene encodes a 145 kDa nuclear, DNA binding protein that contains two domains containing seven and three sets of repeats of the zinc finger motif. During studies to determine the role of the Evi-1 gene in the transformation of human cells, we have found that the Evi-1 gene is uniquely expressed at low levels in HEC-1-A cells and at high levels in HEC-1-B cells, two related human endometrial carcinoma cell lines. cDNA clones were isolated and sequenced from the HEC-1-B cell line. The human gene is highly homologous to the murine gene and shows 91% and 94% homology in nucleotide or amino acid sequence respectively. In addition an alternatively spliced form of the gene was identified that encodes a protein with an internal deletion 315 amino acids including two of the zinc finger repeats. The possible basis for the unique expression of the Evi-1 gene by HEC-1 cells could not be determined by karyotype or Southern blot analysis.

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ISSN
0950-9232
pmid
2115646

Abstract

Retroviral insertional activation of the expression of the Evi-1 is one of the most common events associated with transformation in murine myeloid leukemia. The murine Evi-1 gene encodes a 145 kDa nuclear, DNA binding protein that contains two domains containing seven and three sets of repeats of the zinc finger motif. During studies to determine the role of the Evi-1 gene in the transformation of human cells, we have found that the Evi-1 gene is uniquely expressed at low levels in HEC-1-A cells and at high levels in HEC-1-B cells, two related human endometrial carcinoma cell lines. cDNA clones were isolated and sequenced from the HEC-1-B cell line. The human gene is highly homologous to the murine gene and shows 91% and 94% homology in nucleotide or amino acid sequence respectively. In addition an alternatively spliced form of the gene was identified that encodes a protein with an internal deletion 315 amino acids including two of the zinc finger repeats. The possible basis for the unique expression of the Evi-1 gene by HEC-1 cells could not be determined by karyotype or Southern blot analysis.

Journal

OncogenePubmed

Published: Aug 30, 1990

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