Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transcription driven by the proviral promoter of the Human T-cell Leukemia Virus type I (HTLV-I) is tightly regulated by the Tax1 transactivator. This viral protein potently induces the enhancer activity of a 21 bp motif repeated three times in the promoter. We have previously shown that this induction results from the binding of Tax1 to this enhancer sequence and that this association is mediated by the cellular factor HEB1. In this paper we report the purification of this factor by chromatography and DNA affinity precipitation. The latter method allowed a rapid and efficient purification which led to the identification of two polypeptides with molecular masses of 94- and 67-kDa, named HEB1-p94 and HEB1-p67, respectively. DMS methylation interference and UV crosslinking experiments indicated that both proteins formed different nucleo-protein complexes, but had the same DNA specificity. Study of the interaction of these two proteins with Tax1 showed that only HEB1-p67 can specifically interact with Tax1.
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PMID:Purification by DNA affinity precipitation of the cellular factors HEB1-p67 and HEB1-p94 which bind specifically to the human T-cell leukemia virus type-I 21 bp enhancer. 837 70

p94(fer) is a cytoplasmic and nuclear tyrosine kinase whose function has been linked to cell growth. p94(fer) accumulates at different levels in various cell types and is not detected in pre-B, pre-T and T-cells (Halachmy, S., Bern, O., Schreiber, L., Carmel, M., Sharabi, Y., Shoham, J., Nir, U., 1997. p94(fer) facilitates cellular recovery of gamma irradiated pre-T cells. Oncogene 14, 2871-2880). The fer RNA, encoding p94fer, is transcribed from the FER locus in human rat and mouse. In the present work, a Fer gene transcription initiation point was determined, and the Fer promoter was cloned. A DNA genomic fragment, extending 3698bp upstream of the fer RNA start site, was isolated, sequenced and functionally characterized. A transient transfection assay, carried out in fibroblastic cell lines, revealed the presence of the Fer promoter within the cloned genomic fragment. The Fer promoter contains neither an obvious 'TATA' element nor a putative initiator sequence, but is composed of positive and negative, cis-acting elements. Negative regulation was found to be the main cause for dysfunctioning of the Fer promoter in a T-cell leukemia cell line (Jurkat). The minimal Fer promoter that is still active in fibroblasts consists of an AP1 binding site located 14bp upstream of the fer transcription initiation point. This minimal promoter was not active in the Jurkat T-cell leukemia cells and did not bind AP1 in these cells. Three additional AP1 sites were identified in functional sequences of the Fer promoter. Thus, the availability of AP1 activity may contribute as well to the modulation of the Fer promoter activity. The presumed regulatory role of AP1 in modulating the Fer promoter activity implies a link between cell growth and the Fer gene expression level. Indeed, exposure of fibroblasts to low serum growth conditions reduced the cellular level of the fer RNA.
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PMID:Role of positive and negative regulation in modulation of the Fer promoter activity. 1060 2