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Your search keyword '"Hooper, Martin"' showing total 5 results
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5 results on '"Hooper, Martin"'

1. Mutations in T-cell antigen receptor genes alpha and beta block thymocyte development at different stages

Author

Mombaerts, Peter, Clarke, Alan R., Rudnicki, Michael A., Iacomini, John, Itohara, Shigeyoshi, Lafaille, Juan J., Wang, Lili, Ichikawa, Yoshiaki, Jaenisch, Rudolf, Hooper, Martin L., and Tonegawa, Susumu

Subjects
Antigen receptors, T cell -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Research using mice with mutant T-cell antigen receptor (TCR) genes shows that rearrangement or expression of the TCR-beta gene is necessary and sufficient for differentiation of CD4-CD8-thymocytes into the CD4+CD8+ form and for expanding the pool of thymocytes. Expression of the TCR-alpha gene is irrelevant to these processes. Furthermore, the TCR-alpha and TCR-beta mutation does not hinder development of gamma and delta T-cells.

Published
1992

2. Cystic fibrosis in the mouse by targeted insertional mutagenesis

Author

Dorin, Julia R., Dickinson, Paul, Alton, Eric W.F.W., Smith, Stephen N., Geddes, Duncan M., Stevenson, Barbara J., Kimber, Wendy L., Fleming, Stewart, Clarke, Alan R., Hooper, Martin L., Anderson, Louise, Beddington, Rosa S.P., and Porteous, David J.

Subjects
Cystic fibrosis -- Models, Mice as laboratory animals -- Innovations, Mutagenesis -- Usage, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

A new mouse model for cystic fibrosis (CF) has been devised that should be useful in trials of potential treatments for this deadly autosomal recessive disorder. The new model was produced through mutagenesis or the genetic disruption of the CF transmembrane conductance regulator gene in murine embryonic stem cells. The detection of the characteristic CF pathophysiology in the mice such as abnormal chloride ion transport verified the similarity of the model to human CF.

Published
1992

3. Requirement for a functional Rb-1 gene in murine development

Author

Clarke, Alan R., Maandag, Els Robanus, van Roon, Marian, van der Lugt, Nathalie M.T., van der Valk, Martin, Hooper, Martin L., Berns, Anton, and te Riele, Hein

Subjects
Retinoblastoma -- Genetic aspects, Developmental genetics -- Research, Nervous system -- Abnormalities, Hematopoietic system -- Abnormalities, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

RB-1, a gene the mutation of which has been linked to retinoblastoma, produces different homozygous and heterozygous effects when inactivated in mouse embryos. Heterozygous mice survive to term and exhibit neither physical abnormalities nor the growth of retinoblastoma tumors. On the other hand, homozygous mouse embryos die before birth and exhibit an array of neural and hematopoietic abnormalities.

Published
1992

5. Carcinogen-induced pancreatic lesions in the mouse: effect of Smad4 and Apc genotypes.

Author

Cullingworth J, Hooper ML, Harrison DJ, Mason JO, Sirard C, Patek CE, and Clarke AR

Subjects
Adenomatous Polyposis Coli Protein metabolism, Animals, Cell Division drug effects, Cytoskeletal Proteins metabolism, DNA-Binding Proteins metabolism, Genotype, Immunohistochemistry, In Situ Nick-End Labeling, Mice, Mutation, Pancreatic Neoplasms chemically induced, Proto-Oncogene Proteins metabolism, Signal Transduction drug effects, Smad4 Protein, Trans-Activators metabolism, Transforming Growth Factor beta pharmacology, Wnt Proteins, beta Catenin, Adenomatous Polyposis Coli Protein genetics, Carcinogens toxicity, DNA-Binding Proteins genetics, Methylnitrosourea toxicity, Pancreatic Neoplasms genetics, Pancreatic Neoplasms pathology, Trans-Activators genetics, Zebrafish Proteins
Abstract

Mutations in the tumour suppressor genes SMAD4 (DPC4, deleted in pancreatic cancer locus 4) and adenomatous polyposis coli (APC) have been implicated in the development of pancreatic cancer in humans. Treatment of wild-type, Smad4(+/-), Apc(Min/+) or Apc(Min/+)Smad4(+/-) mice with N-Nitroso-N-Methyl Urea (NMU) results in abnormal foci in pancreatic acinar cells characterized by increased levels of beta-catenin. Previously such foci have been shown to be the precursors of pancreatic neoplasia. Interestingly, only NMU-treated Apc(Min/+)Smad4(+/-) mice exhibit a significant increase in abnormal pancreas, which was found to be due to increased number of abnormal foci rather than increased focus size. A range of foci sizes were analysed, but only smaller abnormal foci were characterized by morphological nuclear atypia. These studies suggest functional co-operation between TGF-beta and Wnt signalling pathways in the suppression of pancreatic tumorigenesis in the mouse.

Published
2002
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