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S Oestreich

Publications and source records attributed to S Oestreich.

6 recordsLinked to original sources
PubMed2000

Identification of human Rap1: implications for telomere evolution.

It has been puzzling that mammalian telomeric proteins, including TRF1, TRF2, tankyrase, and TIN2 have no recognized orthologs in budding yeast. Here, we describe a human protein, hRap1, that is an ortholog of the yeast telomeric protein, scRap1p. hRap1 has three conserved sequence motifs in common with scRap1, is located at telomeres, and affects telomere length. However, while scRap1 binds telomeric DNA directly, hRap1 is recruited to telomeres by TRF2. Extending the comparison of telomeric proteins to fission yeast, we identify S. pombe Taz1 as a TRF ortholog, indicating that TRFs are conserved at eukaryotic telomeres. The data suggest that ancestral telomeres, like those of vertebrates, contained a TRF-like protein as well as Rap1. We propose that budding yeast preserved Rap1 at telomeres but lost the TRF component, possibly concomitant with a change in the telomeric repeat sequence.

Amino Acid Sequence↗
PubMed1978

[Role of inflammatory cellular infiltrates in the pathogenesis of human coronary arteriosclerosis (author's transl)].

The ramus interventricularis anterior of the arteria coronaria cordis sinistra and the initial part of the arteria coronaria cordis dextra of 125 human patients aged between 20 and 90 years were studied for the occurrence and localisation of inflammatory cellular infiltrates in the vessel walls. A correlation between a pronounced inflammatory cellular infiltration and the presence and degree of severity of coronary arteriosclerosis was established. An inflammatory or immunpathologic cause of coronary arteriosclerosis is rejected. The highest incidence of inflammatory infiltrates was observed in the adventitia within the plaque area. Isolated macrophages were found to be present in all vessel wall layers and age groups.

Adolescent↗
PubMed1976

Comparative histological and morphometrical studies into the relevance of intimal thickening to coronary sclerosis.

It was found by comparative histological and morphometrical studies, carried out on 125 human hearts of different age (20-90 years) and sex, that there exist critical limiting ranges of intima thickness and the intima/media relationship (IMR) for diffuse intimal thickening and the preatheroma phase of arteriosclerosis. Since furthermore a maximum and a minimum intima thickness as relating to diffuse intimal thickening could be determined, it is assumed that the location and formation of arteriosclerotic plaques is determined by the degree of so-called diffuse intimal thickening. It follows from these findings that postnatal intimal proliferation represents a potential prearteriosclerotic lesion of the intima, and that progressive intimal thickening supports the arteriosclerotic alteration of the intima, leading, through an extensive necrosis of the intima, to the atheroma phase.

Adult↗