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Your search keyword '"van der Horst, G T J"' showing total 18 results
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18 results on '"van der Horst, G T J"'

3. Molecular Basis of DNA Repair Mechanisms and Syndromes

Author

Weeda, G., de Boer, J., Donker, I., de Wit, J., Winkler, S. B., van der Horst, G. T. J., Vermeulen, W., Bootsma, D., Hoeijmakers, J. H. J., Schlag, P. M., editor, Senn, H.-J., editor, Diehl, V., editor, Parkin, D. M., editor, Rajewsky, M. F., editor, Rubens, R., editor, Wannenmacher, M., editor, Schwab, Manfred, editor, Rabes, Hartmut M., editor, Munk, Klaus, editor, and Hofschneider, Hans Peter, editor

Published
1998
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7. The nucleotide excision repair protein XPC is essential for bulky DNA adducts to promote interleukin-6 expression via the activation of p38-SAPK

Author

Schreck, I, primary, Grico, N, additional, Hansjosten, I, additional, Marquardt, C, additional, Bormann, S, additional, Seidel, A, additional, Kvietkova, D L, additional, Pieniazek, D, additional, Segerbäck, D, additional, Diabaté, S, additional, van der Horst, G T J, additional, Oesch-Bartlomowicz, B, additional, Oesch, F, additional, and Weiss, C, additional

Published
2015
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10. Reduction in mesenchymal stem cell numbers in premature aging DNA repair deficient TTD mice

Author

Nicolaije, C., van der Eerden, B. C. J., Pols, H. A. P., Hoeijmakers, J. H. J., van der Horst, G. T. J., van Leeuwen, J. P. T., Nicolaije, C., van der Eerden, B. C. J., Pols, H. A. P., Hoeijmakers, J. H. J., van der Horst, G. T. J., and van Leeuwen, J. P. T.

Abstract

Background: Mice carrying mutations in DNA repair genes often show signs of accelerated ageing and therefore can be used as a model system to study age related diseases like osteoporosis. It has been shown that TTD mice, carrying a mutation in the nucleotide excision repair gene XPD (xeroderma pigmentosa group D), display features of ageing related osteoporosis as well as adipose tissue hypoplasia. Since both cell types involved, osteoblasts as well as adipocytes, arise from the same mesenchymal stem cell population, the aim of the current project was to study the number, proliferation and differentiation potential of these cells in TTD compared to wild type (WT) mice. This might provide us with useful information concerning the mechanism behind age-related osteoporosis and the loss of adipose tissue. Methods: Bone marrow from old TTD and WT mice was cultured under osteogenic or adipogenic conditions and analysed for alkaline phosphatase activity (ALP), mineralisation (osteoblast) and lipid deposition (adipocyte). Results: Under osteogenic conditions the number of ALP-positive colonies after 9 and 14 days of culture was significantly decreased (p=0.02) in TTD compared to WT mice. The rate at which new ALP-positive colonies are formed between day 9 and day 14 of culture has not changed between TTD and WT mice, indicating that the decrease in colony number is not due to a delay in differentiation. Mineralisation of ALP-positive colonies did not seem to be affected, with a borderline significant decrease on day 14 at the onset of mineralisation but no significant changes on day 21 of culture. Lipid deposition was strongly reduced in TTD compared to WT mice (p=0.01) after 35 days of culture. Conclusions: The observed reduction in osteoblast and adipocyte differentiation indicates a reduction of mesenchymal stem cell numbers in TTD mice. This reduction in mesenchymal stem cell numbers and the corresponding decline in osteoblast dif

Published
2007

11. Accelerated Bone Aging in Dna Repair Deficient Trichothiodystrophy Mice

Author

Diderich, K. E. M., Waarsing, J. H., Buurman, C. J., Brandt, R. M. C., De Jong, F. H., Hoeijmakers, J. H. J., Weinans, H., Van der Horst, G. T. J., Van Leeuwen, J. P., Diderich, K. E. M., Waarsing, J. H., Buurman, C. J., Brandt, R. M. C., De Jong, F. H., Hoeijmakers, J. H. J., Weinans, H., Van der Horst, G. T. J., and Van Leeuwen, J. P.

Published
2004

15. Mammalian nucleotide excision repair and syndromes

Author

Vermeulen, W., primary, de Boer, J., additional, Citterio, E., additional, van Gool, A. J., additional, van der Horst, G. T. J., additional, Jaspers, N. G. J., additional, de Laat, W. L., additional, Sijbers, A. M., additional, van der Spek, P. J., additional, Sugasawa, K., additional, Weeda, G., additional, Winkler, G. S., additional, Bootsma, D., additional, Egly, J.-M., additional, and Hoeijmakers, J. H. J., additional

Published
1997
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16. Identification and in VitroReconstitution of Lysosomal Neuraminidase from Human Placenta

Author

van der Horst, G T J, Galjart, N J, d'Azzo, A, Galjaard, H, and Verheijen, F W

Abstract

Lysosomal neuraminidase from human placenta has been obtained in its active form by association of an inactive neuraminidase polypeptide with β-galactosidase and the protective protein. Using a specific antiserum, we have now identified a 66-kDa protein as the inactive neuraminidase polypeptide. It is specifically recognized on immunoblots only in its nonreduced state, and it coprecipitates with neuraminidase activity. The 66-kDa polypeptide is substantially glycosylated (38-kDa protein core with 7–14 N-linked oligosaccharide chains), a feature characteristic of lysosomal integral membrane proteins. Specific removal of the 66-kDa neuraminidase polypeptide from glycoprotein preparations prevents the generation of neuraminidase activity. Removal of β-galactosidase or destruction of the protective protein also hinders the formation of active neuraminidase. Reconstitution of neuraminidase activity is observed after mixing glycoprotein preparations, depleted in different components of the β-galactosidase-neuraminidase-protective protein complex, indicating that all three components of the complex are required for neuramindase activity. Association of the neuraminidase polypeptide and the protective protein generates unstable neuraminidase activity, whereas association with β-galactosidase is required for stability.

Published
1989
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18. The effect of DNA repair defects on reproductive performance in nucleotide excision repair (NER) mouse models: an epidemiological approach.

Author

Tsai PS, Nielen M, van der Horst GT, Colenbrander B, Heesterbeek JA, and van Vlissingen JM

Subjects
Animals, Breeding, DNA Repair Enzymes, Epidemiologic Studies, Female, Humans, Litter Size, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Poly-ADP-Ribose Binding Proteins, Seasons, DNA Helicases genetics, DNA Repair physiology, DNA-Binding Proteins genetics, Disease Models, Animal, Proteins genetics, Reproduction physiology, Xeroderma Pigmentosum Group A Protein genetics
Abstract

In this study, we used an epidemiological approach to analyze an animal database of DNA repair deficient mice on reproductive performance in five Nucleotide Excision Repair (NER) mutant mouse models on a C57BL/6 genetic background, namely CSA, CSB, XPA, XPC [models for the human DNA repair disorders Cockayne Syndrome (CS) and xeroderma pigmentosum (XP), respectively] and mHR23B (not associated with human disease). This approach allowed us to detect and quantify reproductive effects based on a relatively small number of matings. We measured and quantified the scale of the effect between factors that might influence reproductive performance (i.e. age at co-housing, seasons) and reproductive parameters (i.e. litter size and pairing-to-birth interval -'pbi'). Besides, we detected and quantified the differences in reproductive performance between wild type mice and heterozygous/homozygous NER mutant mice. From our analyses, we found impaired reproduction in heterozygous and homozygous knock out mice; in particular, reduced litter size and lengthened pbi was related to the NER mutation-mHR23B, in heterozygous couples, even if they were otherwise phenotypically normal. Heterozygous mHR23B couples produced a 6.6-fold lower number of mHR23B(-/-) pups than indicated by Mendelian expectation; other genetic deficiencies studied were not statistically significant from each other or wild type controls. We concluded that careful epidemiological evaluations by analysis of animal database could provide reliable information on reproductive performance and detect deviations that would remain unnoticed without this. Also, some managerial aspects of mouse breeding could be evaluated.

Published
2005
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