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Fli-1b is generated by usage of differential splicing and alternative promoter.
Oncogene. 1998 Sep 03; 17(9):1149-57.O

Abstract

The proto-oncogene Fli-1, a member of Ets family is rearranged or activated through proviral integration in erythroleukemias, induced by Friends' Murine Leukemia Virus. The DNA binding domain (ETS domain) of Fli-1 is fused to the RNA binding domain of EWS by t(11q24:22q12) chromosomal translocation in Ewing's sarcoma and primitive neuroectodermal tumors. Screening of human cDNA libraries has identified two different 5'-termini and alternatively spliced forms of the human Fli-1 gene (Fli-1b), suggesting the possible existence of two independent promoters. The genomic sequence adjacent to the alternate exon of human Fli-1b gene shows functional promoter activity when cloned in promoter-less CAT expression vector and transfected into QT-6 cells. The transcription initiation (CAP) site and minimum promoter region necessary for function were localized. The 5'-flanking regions of human Fli-1b and mouse Fli-1 show 80% homology suggesting conserved promoter regulatory elements. The Fli-1b 5'-flanking sequence lacks canonical TATA or CCAAT boxes but contains a partially conserved TATA-like sequence at position 242. Several transcription factor binding sequences like ATF/CREB, E2A-PBX1, EBP, PEA-3, ETS-2, Sp-1, c-Myc, TBP, GATA-1 and Oct-3 were conserved in the promoter sequence. Functional promoter assays revealed that Fli-1b promoter shows very strong transcriptional activation compared to Fli-1 promoter. We also showed that variant Fli-1b has transcriptional activation properties similar to those of Fli-1. Fli-1b and Fli-1 show differential expression in various hematopoietic cell lines. This differential expression and promoter activities of Fli-1 and Fli-1b suggests that several mechanisms are involved in Fli-1 gene regulation which are mediated by many transcription factors.

Authors+Show Affiliations

Department of Human Genetics, Allegheny University of the Health Sciences, Philadelphia, Pennsylvania 19102, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

9764825

Citation

Dhulipala, P D., et al. "Fli-1b Is Generated By Usage of Differential Splicing and Alternative Promoter." Oncogene, vol. 17, no. 9, 1998, pp. 1149-57.
Dhulipala PD, Lee L, Rao VN, et al. Fli-1b is generated by usage of differential splicing and alternative promoter. Oncogene. 1998;17(9):1149-57.
Dhulipala, P. D., Lee, L., Rao, V. N., & Reddy, E. S. (1998). Fli-1b is generated by usage of differential splicing and alternative promoter. Oncogene, 17(9), 1149-57.
Dhulipala PD, et al. Fli-1b Is Generated By Usage of Differential Splicing and Alternative Promoter. Oncogene. 1998 Sep 3;17(9):1149-57. PubMed PMID: 9764825.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fli-1b is generated by usage of differential splicing and alternative promoter. AU - Dhulipala,P D, AU - Lee,L, AU - Rao,V N, AU - Reddy,E S, PY - 1998/10/9/pubmed PY - 1998/10/9/medline PY - 1998/10/9/entrez SP - 1149 EP - 57 JF - Oncogene JO - Oncogene VL - 17 IS - 9 N2 - The proto-oncogene Fli-1, a member of Ets family is rearranged or activated through proviral integration in erythroleukemias, induced by Friends' Murine Leukemia Virus. The DNA binding domain (ETS domain) of Fli-1 is fused to the RNA binding domain of EWS by t(11q24:22q12) chromosomal translocation in Ewing's sarcoma and primitive neuroectodermal tumors. Screening of human cDNA libraries has identified two different 5'-termini and alternatively spliced forms of the human Fli-1 gene (Fli-1b), suggesting the possible existence of two independent promoters. The genomic sequence adjacent to the alternate exon of human Fli-1b gene shows functional promoter activity when cloned in promoter-less CAT expression vector and transfected into QT-6 cells. The transcription initiation (CAP) site and minimum promoter region necessary for function were localized. The 5'-flanking regions of human Fli-1b and mouse Fli-1 show 80% homology suggesting conserved promoter regulatory elements. The Fli-1b 5'-flanking sequence lacks canonical TATA or CCAAT boxes but contains a partially conserved TATA-like sequence at position 242. Several transcription factor binding sequences like ATF/CREB, E2A-PBX1, EBP, PEA-3, ETS-2, Sp-1, c-Myc, TBP, GATA-1 and Oct-3 were conserved in the promoter sequence. Functional promoter assays revealed that Fli-1b promoter shows very strong transcriptional activation compared to Fli-1 promoter. We also showed that variant Fli-1b has transcriptional activation properties similar to those of Fli-1. Fli-1b and Fli-1 show differential expression in various hematopoietic cell lines. This differential expression and promoter activities of Fli-1 and Fli-1b suggests that several mechanisms are involved in Fli-1 gene regulation which are mediated by many transcription factors. SN - 0950-9232 UR - https://www.unboundmedicine.com/medline/citation/9764825/Fli_1b_is_generated_by_usage_of_differential_splicing_and_alternative_promoter_ L2 - https://doi.org/10.1038/sj.onc.1202030 DB - PRIME DP - Unbound Medicine ER -