| 1. |
- Andersson, A, et al.
(författare)
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Genes for C4b-binding protein alpha- and beta-chains (C4BPA and C4BPB) are located on chromosome 1, band 1q32, in humans and on chromosome 13 in rats
- 1990
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Ingår i: Somatic Cell and Molecular Genetics. - 0740-7750. ; 16:5, s. 493-500
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Tidskriftsartikel (refereegranskat)abstract
- C4b-binding protein is involved in the regulation of the complement system. It is a multimeric protein composed of seven identical alpha-chains and a single copy of a unique beta-chain. The latter was identified only recently and its structure determined by cDNA cloning. Both subunits in C4b-binding protein belong to the same superfamily of proteins composed predominantly of tandemly arranged short consensus repeats (SCR) approximately 60 amino acid residues in length. The gene for the human alpha-chain is known to be located in a gene cluster on chromosome 1, band 1q32, which is called the regulators of complement activation (RCA) gene cluster. We have used cDNA probes for both alpha- and beta-chains of human C4b-binding protein to localize their genes with an in situ hybridization technique. We find the genes for both chains to be located on chromosome 1, band 1q32, in the human. This suggests that the beta-chain gene is also a member of the RCA gene cluster and that the alpha- and beta-chain genes are located close to each other. The cDNA probes for the alpha- and beta-chains also were used to screen mouse-rat somatic cell hybrids using Southern blotting to localize their genes in the rat. Both the alpha- and beta-chain genes were shown to be located on chromosome 13 in the rat. These are the second and third genes to be located on rat chromosome 13, and the results suggest that the genes for the alpha- and beta-chains together with the gene for coagulation factor V represent a conserved chromosomal region in rat and man.
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| 2. |
- Dahlbäck, Björn, et al.
(författare)
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Assignment of gene for coagulation factor V to chromosome 1 in man and to chromosome 13 in rat
- 1988
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Ingår i: Somatic Cell and Molecular Genetics. - 0740-7750. ; 14:5, s. 14-509
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Tidskriftsartikel (refereegranskat)abstract
- Two different factor V cDNA fragments were used as hydridization probes in the chromosomal assignment of the human and rat factor V genes. A 1.6-kb EcoRI fragment was used as a hybridization probe to analyze a panel of human-rodent somatic cell hybrids. Cosegregation of factor V specific DNA restriction fragments with human chromosome 1 was observed. In addition, a panel of rat-mouse somatic cell hybrids was analyzed with another human factor V cDNA probe to localize the gene for rat coagulation factor V. In the rat, the gene for coagulation factor V was found to be located in chromosome 13. This is the first gene in the rat to be localized to chromosome 13.
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| 3. |
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| 4. |
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| 5. |
- Klinga-Levan, K, et al.
(författare)
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The rat gene map 1995
- 1995
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Rapport (övrigt vetenskapligt/konstnärligt)
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| 6. |
- Klinga-Levan, K, et al.
(författare)
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The rat gene map 1996
- 1996
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Rapport (övrigt vetenskapligt/konstnärligt)
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| 7. |
- Levan, G, et al.
(författare)
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The rat gene map
- 1998
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Ingår i: ILAR journal. - : Institute for Laboratory Animal Research. - 1084-2020 .- 1930-6180. ; 39, s. 132-137
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Tidskriftsartikel (refereegranskat)
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| 8. |
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| 11. |
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| 13. |
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| 14. |
- Levan, G, et al.
(författare)
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Recent advances in rat genomics
- 1997
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Ingår i: Transplantation Proceedings. - : Elsevier Inc.. - 0041-1345 .- 1873-2623. ; 29:3, s. 1759-1760
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Tidskriftsartikel (refereegranskat)abstract
- The rat has been the model organism of choice for many researchers, for example, in physiology, immunology, and behavior research. Unfortunately, rat genetics have been lagging behind (compared to the mouse), but in the last decade considerable progress has been made in the field of “rat genomics,” as will be briefly reviewed below.
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| 15. |
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| 16. |
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| 17. |
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| 18. |
- Walentinsson, A, et al.
(författare)
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Independent amplification of two gene clusters on chromosome 4 in rat endometrial cancer: identification and molecular characterization.
- 2001
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Ingår i: Cancer research. - 0008-5472. ; 61:22, s. 8263-73
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Tidskriftsartikel (refereegranskat)abstract
- The BDII rat is genetically predisposed to hormone-dependent endometrial adenocarcinoma and was used to model human cancer. Tumors arising spontaneously in strain crosses involving BDII rats were analyzed by means of comparative genome hybridization. The most common aberration was amplification of the proximal region of rat chromosome 4, centered around bands q12-q22. The copy numbers of 15 cancer-related genes from the region were examined in tissue cultures of 11 endometrial carcinomas (10 endometrial adenocarcinomas and 1 endometrial squamous cell carcinoma) and one peritoneal mesothelioma. Amplification in rat chromosome 4 was detected in six tumors (50%), five of which carried two separate amplified regions, situated at 4q12-q13 and 4q21-q22, interrupted by a nonamplified segment at 4q13-q21.1. The genes Cdk6 (cyclin-dependent kinase 6) and Met (hepatocyte growth factor receptor) were located in the core of each amplified region and were amplified most recurrently and at the highest levels among the genes tested. Using fluorescence in situ hybridization on tumor metaphases, it was observed that the amplified Cdk6 and Met sequences were situated on typical homogeneously staining regions (HSRs). In three tumors, both genes were amplified in the same HSRs, whereas in two tumors, the amplified sequences of each gene were situated in separate HSRs. In addition, Cdk6 and Met amplification was consistently associated with a corresponding increase in gene expression, suggesting that the two genes might represent the targets for the amplifications. In the sixth tumor, which carried amplified sequences of Met but not of Cdk6, coexpression of Met and the normally silent hepatocyte growth factor gene (Hgf; the ligand of Met) was observed. This finding suggests that an autocrine signaling circuit might be operating in this particular tumor. Taken together, our findings suggest that up-regulation of Cdk6 and/or Met may contribute to the development of endometrial cancers in the BDII rat.
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