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Biomedical subjects

R H Deprez

Publications and source records attributed to R H Deprez.

5 recordsLinked to original sources
PubMed1997

Developmental changes in rat cardiac DNA, RNA and protein tissue base: implications for the interpretation of changes in gene expression.

During cardiac development the expression levels of many genes change as determined by Northern blot, dot blot, RNase protection, quantitative RT-PCR. Western blot or immunoprecipitation analyses. It is not always realized that the total amount of RNA or protein per gram of heart, dubbed tissue base, may change significantly during development as well. If this would be the case, this has to be taken into account. So far, the (changing) tissue base has not been established during cardiac development. To this end developmental profiles of cardiac DNA, RNA and protein concentration were determined in rats ranging in age from embryonic day 13 until neonatal day 121. The profiles show significant development changes in each parameter, that closely match the distinct growth phases of the developing heart and provide the parameters that are essential for an adequate interpretation of changes in the amount of a distinct mRNA and/or protein. In a comparison between in situ hybridization and Northern blot analysis it is demonstrated that the same developmental profile leads to an almost opposite conclusion depending on whether or not the changing tissue base is taken into account. These findings are of great interest for studies aimed at unravelling the molecular mechanisms underlying the regulation of gene expression during cardiac development.

Age Factors↗
PubMed1995

Characterization of four novel CAG repeat-containing cDNAs.

Stretches of CAG nucleotides coding for the amino acid glutamine are an important feature of many transcription factors and genes that are involved in neurodegenerative disorders. In an attempt to isolate CAG repeat-containing cDNAs expressed in nervous tissue, we screened a human fetal brain cDNA library with a probe containing a CAG repeat. Five different clones were characterized and found to contain CAG repeats. Sequence data revealed that four of these cDNAs were derived from novel genes. These cDNAs were designated CAG6, CAG12, CAG24, and CAG40 and were found to correspond to transcripts of 5.0, 7.5, 4.4, and 15 kb, respectively. The genes encoding CAG6, CAG12, CAG24, and CAG40 were assigned to chromosomes 12, 16, X, and 12, respectively. For the 5th gene, CAG26/pRHpA, a localization on two different chromosomes was established: 16 and X. None of the repeats showed any length polymorphisms in human DNA.

Base Sequence↗
PubMed1994

Familial anaplastic ependymoma: evidence of loss of chromosome 22 in tumour cells.

A family with anaplastic ependymomas, histologically verified in three cases and neuroradiologically suggested in a fourth, is presented. Two healthy brothers both had two affected sons. All four male patients were younger than 5 years at the time of diagnosis. Two boys died before the age of 3 years. Genotype analysis (with polymorphic DNA markers for chromosome 22 and interphase cytogenetic analysis) of one of the tumours showed a subpopulation of tumour cells with monosomy of (part of) chromosome 22. Non-neoplastic cells of this patient showed a normal karyotype. These findings give further evidence for the role of a tumour suppressor gene on chromosome 22 in the pathogenesis of familial ependymal tumours.

Brain Neoplasms↗