The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Mice deficient in cystathionine beta-synthase: animal models for mild and severe homocyst(e)inemia.
Open accessAbstract
Studies by various investigators have indicated that elevated levels of plasma homocyst(e)ine are strongly associated with the occurrence of occlusive vascular diseases. With the eventual aim of determining whether or not elevated plasma homocyst(e)ine concentrations are directly causative of cardiovascular diseases, we have generated mice that are moderately and severely homocyst(e)inemic. Homologous recombination in mouse embryonic stem cells was used to inactivate the cystathionine beta-synthase [L-serine hydrolyase (adding homocysteine), EC 4.2.1.22] gene. Homozygous mutants completely lacking cystathionine beta-synthase were born at the expected frequency from matings of heterozygotes, but they suffered from severe growth retardation and a majority of them died within 5 weeks after birth. Histological examination showed that the hepatocytes of homozygotes were enlarged, multinucleated, and filled with microvesicular lipid droplets. Plasma homocyst(e)ine levels of the homozygotes were approximately 40 times normal. These mice, therefore, represent a model for severe homocyst(e)inemia resulting from the complete lack of cystathionine beta-synthase. Heterozygous mutants have approximately 50% reduction in cystathionine beta-synthase mRNA and enzyme activity in the liver and have twice normal plasma homocyst(e)ine levels. Thus, the heterozygous mutants are promising for studying the in vivo role of elevated levels of homocyst(e)ine in the etiology of cardiovascular diseases.
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Plump, A. S., Smith, J. D., Hayek, T., Aalto-Setälä, K., Walsh, A., Verstuyft, J. G., Rubin, E. M., & Breslow, J. L. (1992) · Cell · doi:10.1016/0092-8674(92)90362-g · Cited by 2,263
Spontaneous Hypercholesterolemia and Arterial Lesions in Mice Lacking Apolipoprotein E
Zhang, S. H., Reddick, R. L., Piedrahita, J. A., & Maeda, N. (1992) · Science · doi:10.1126/science.1411543 · Cited by 2,237
Self-citationPiedrahita, J. A., Zhang, S. H., Hagaman, J. R., Oliver, P. M., & Maeda, N. (1992) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.89.10.4471 · Cited by 944
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Cited by
Schmidt, J. V., Su, G. H., Reddy, J. K., Simon, M. C., & Bradfield, C. A. (1996) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.93.13.6731 · Cited by 891
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Paul, B. D., & Snyder, S. H. (2012) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3391 · Cited by 853
Chen, Z. (2001) · Human Molecular Genetics · doi:10.1093/hmg/10.5.433 · Cited by 607
Neural tube defects and folate: case far from closed
Blom, H. J., Shaw, G. M., den Heijer, M., & Finnell, R. H. (2006) · Nature Reviews Neuroscience · doi:10.1038/nrn1986 · Cited by 562
Physiological roles of hydrogen sulfide in mammalian cells, tissues, and organs
Cirino, G., Szabo, C., & Papapetropoulos, A. (2023) · Physiological Reviews · doi:10.1152/physrev.00028.2021 · Cited by 553
Metadata
- Authors
- Watanabe, M., Osada, J., Aratani, Y., Kluckman, K., Reddick, R., Malinow, M. R., & Maeda, N.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1995-02-28
- Volume
- 92
- Issue
- 5
- Pages
- 1585-1589
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2054847530
- Cited by
- 569
- References
- 3
- FWCI
- 5.42
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Watanabe, M., Osada, J., Aratani, Y., Kluckman, K., Reddick, R., Malinow, M. R., & Maeda, N. (1995). Mice deficient in cystathionine beta-synthase: animal models for mild and severe homocyst(e)inemia. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.92.5.1585
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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