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H Delhez

Publications and source records attributed to H Delhez.

6 recordsLinked to original sources
PubMed1998

Introduction of a normal retinoblastoma (Rb) gene into Rb-deficient lymphoblastoid cells delays tumorigenicity in immunodefective mice.

Inactivation of the Rb susceptibility gene occurs in various human cancers and has been associated with tumorigenicity. Rb gene is inactivated in 30% of acute leukaemias. The effect of Rb protein expression was assessed in the lymphoblastoid cell line IM-9 defective for Rb protein, after stable transfection with a wild-type Rb gene. The Rb transgene was under the control of the MoMuLv-LTR. Protein expression by the transduced cells was confirmed by Western blot and flow cytometry analyses. Compared to the parental cell line, growth rate remained unchanged in the Rb transfected clones. In SCID mice however, tumor formation originating from these clones was delayed. The current data suggest therefore that, in this Rb-defective haematopoietic cell line, Rb expression correlates with reduced tumorigenicity but not with reduced growth rate.

Animals↗
PubMed1994

Promoter function of the human glucose-6-phosphate dehydrogenase gene depends on two GC boxes that are cell specifically controlled.

Human glucose-6-phosphate dehydrogenase is expressed in all cells by a housekeeping gene whose regulatory 5'-flanking sequence includes at least nine GC boxes. By transient transfection of HeLa and HepG2 cells with constructs containing glucose-6-phosphate dehydrogenase gene regions linked to a reporter gene, we have now delineated the core promoter and have located upstream stimulatory and inhibitory sequences. By mutational analysis, we demonstrate that the activity of the core promoter requires two out of seven GC boxes. We show that stimulatory protein 1 (Sp1)-related factors and activator protein 2 (AP-2)-related proteins bind to these two boxes in band-shift experiments. One point mutation that affects the binding of only the Sp1-related factors to one or both boxes causes a marked decrease of promoter activity in HepG2 cells but not in HeLa cells. We conclude that (a) two out of many seemingly redundant GC boxes are necessary to drive a G+C-rich housekeeping promoter; (b) factors that bind to GC boxes may exert cell-type-specific regulation of housekeeping gene promoter activity; (c) point mutations in the promoter of the glucose-6-phosphate dehydrogenase gene can inhibit its transcription.

Base Sequence↗
PubMed1984

Discrepancies between histological and physical methods for trace element mapping in the rat brain.

This paper contains a comparison between four experimental methods for the detection of trace metals in biological tissues, e.g. autoradiography, dithizone-, Timm-staining and microPIXE (Particle Induced X-ray Emission). As research object the hippocampus of the rat was chosen and mainly the Zn-distribution in the fascia dentata has been examined. The comparison was judged on four criteria: spatial resolution, specificity, quantification and influence of the protein binding of the metal on the outcome of each method. Some additional Timm and microPIXE experiments have been performed to compare the metal concentrations for both normal and Zn-deficient rats. The Zn/Cu ratio for both kinds of rats were calculated and some striking differences in the concentrations were obtained. The Zn/Cu ratio for a normal rat was found to be about 40% higher than for a deficient one.

Animals↗
PubMed1983

Autoradiographic demonstration of the copper-accumulating tissues in mice with a defect homologous to Menkes' Kinky Hair disease.

Mutated Brindled mice have a genetic defect homologous to the human disorder Menkes' or Kinky Hair disease. These animals were used to survey the tissues in which copper accumulates as result of this defect. Heterozygous and unaffected animals were i.p. injected with radio-copper (64Cu). Sites of pathological 64Cu accumulation were visualized by whole body autoradiography. Apart from the tissues already known to accumulate copper, particularly the kidneys, pathological accumulations were also found in a number of other tissues. It is concluded that in Menkes' disease copper accumulates in epithelioid cells.

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