Cloning and characterization of the TATA‐less promoter from the human GFI1 Proto‐oncogene

Abstract

The growth factor independent 1 (GFI1) gene encodes a zinc finger protein which acts as a transcriptional repressor and confers growth factor independence on tumor cells, as suggested by the study of its mouse ortholog, Gfi1. We previously isolated the human GFI1 gene but no information about the structure and location of the promotor of this gene has been reported. In this study we have cloned and characterized the human GFI1 promoter. The nucleotide sequence of the promoter region is GC‐rich and does not contain a typical TATA or CAAT box. Several Sp1 sites are present and computer predictions indicate that either of the two Sp1 sites might serve as the sites for transcription initiation. Analysis of various lengths of the promoter region using the luciferase reporter assay identifies a functional promoter that is active in NIH3T3 cells. The strongest activity lies within a region 312–602 basepairs upstream from the translation start site.

Transcriptional Control of Spliced and Unspliced Human T-Cell Leukemia Virus Type 1 bZIP Factor ( HBZ ) Gene

“…This fact might account for the scattered transcription start sites of sHBZ. Additionally, it was previously reported that Sp1 is critical for many TATA-less promoters (3,19). In this study, the sHBZ gene promoter certainly fit this pattern.…”

High levels of the onco-protein Gfi-1 accelerate T-cell proliferation and inhibit activation induced T-cell death in Jurkat T-cells

“…In the primary murine T-cells studied here, the activation of Erk1/2 by phosphorylation occurs directly as a consequence of stimulation with anti-CD3 antibodies and declines after 6 h. Our ®nding that G®-1 becomes detectable in activated T-cells shortly after the peak of Erk1/2 activation suggests that the regulation of the G®-1 gene is an outcome of Erk1/2 activation. This is supported by recent ®ndings, which suggested the existence of several putative binding sites of the Fos/Jun heterodimer (AP-1) within the G®-1 promoter sequence (Liu and Cowell, 2000). Moreover, the G®-1 promoter itself contains a G®-1 binding site and although further evidence has to show whether this bears any signi®cance it already oers an explanation for the transient upregulation of G®-1 mRNA expression observed in splenocytes upon Con A treatment (shown here) or in puri®ed T-cells after phorbol ester stimulation (RoÈ del et al, 2000).…”

Transcription factor Gfi-1 induced by G-CSF is a negative regulator of CXCR4 in myeloid cells

“…We observed sustained STAT3 phosphorylation, increased expression of Gfi-1, and decreased expression of CXCR4 in 32Dcl3 cells after exposure to G-CSF and have identified a putative STAT-binding site (attttaTTCCtaaaaattt) within the human Gfi-1 promoter. 49 Yeast 2-hybrid screens detected physical interaction between the STAT3 inhibitor PIAS3 and Gfi-1, 50 raising the possibility that the STAT3-Gfi-1 axis may participate in modulation of G-CSF-induced CXCR4 expression and neutrophil mobilization. Previous analyses of the human CXCR4 promoter identified putative consensus sequences for binding of different transcription factors, 51 and subsequent studies have documented the binding of certain transcription factors to the CXCR4 promoter, including YY1, 52,53 NF-B, 54 p53, 54,55 and the von Hippel-Lindau tumor suppressor protein pVHL.…”