Change search
Refine search result
12 51 - 60 of 60
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • harvard-cite-them-right
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Rows per page
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sort
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
Select
The maximal number of hits you can export is 250. When you want to export more records please use the Create feeds function.
  • 51.
    Ståhl, Fredrik
    et al.
    University of Borås, Faculty of Caring Science, Work Life and Social Welfare.
    Martinsson, T
    Dahllöf, B
    Levan, G
    Amplification and over-expression of the P-glycoprotein genes and differential amplification of three other genes in SEWA murine multidrug-resistant cells1988In: Hereditas, ISSN 0018-0661, E-ISSN 1601-5223, Vol. 108, no 2, p. 251-258Article in journal (Refereed)
  • 52.
    Ståhl, Fredrik
    et al.
    University of Borås, Faculty of Caring Science, Work Life and Social Welfare.
    Sandberg, P
    Martinsson, T
    Skoog, J
    Dahllöf, B
    Wettergren, Y
    Bjursell, G
    Levan, G
    Isolation of selectively amplified DNA sequences from multidrug-resistant SEWA cells1987In: Hereditas, ISSN 0018-0661, E-ISSN 1601-5223, Vol. 106, no 1, p. 97-105Article in journal (Refereed)
  • 53.
    Ståhl, Fredrik
    et al.
    University of Borås, Faculty of Caring Science, Work Life and Social Welfare.
    Wettergren, Y
    Levan, G
    Amplicon structure in multidrug-resistant murine cells: A non-rearranged region of genomic DNA corresponding to large circular DNA1992In: Molecular and Cellular Biology, ISSN 0270-7306, E-ISSN 1098-5549, Vol. 12, no 3, p. 1179-1187Article in journal (Refereed)
    Abstract [en]

    Multidrug resistance (MDR) in tumor cell lines is frequently correlated with amplification of one or more mdr genes. Usually the amplified domain also includes several neighboring genes. Using pulsed-field gel electrophoresis, we have established a restriction map covering approximately 2,200 kb in the drug-sensitive mouse tumor cell line TC13K. The mapped region is located on mouse chromosome 5 and includes the three mdr genes, the gene for the calcium-binding sorcin protein, and a gene with unknown function designated class 5. Long-range maps of the amplified DNA sequences in five of six MDR sublines that had been independently derived from TC13K generally displayed the same pattern as did the parental cell line. All six MDR sublines exhibited numerous double minutes, and one of them displayed a homogeneously staining region in a subpopulation. Large circular molecules, most likely identical to one chromatid of the double minutes, were detected in four of the sublines by linearization with gamma irradiation. The size of the circles was about 2,500 kb, which correlated to a single unit of the amplified domain. We therefore propose that in four independent instances of MDR development, a single unit of about 2,500 kb has been amplified in the form of circular DNA molecules. The restriction enzyme map of the amplified unit is unchanged compared with that of the parental cell line, whereas the joining sites of the circular DNA molecules are not identical but are in the same region.

  • 54. Ståhl, Fredrik
    et al.
    Wettergren, Y
    Levan, G
    Amplification and overexpression of the mouse mdria gene in nine independently selected multidrug-resistant SEWA murine cell lines1993In: Hereditas, ISSN 0018-0661, E-ISSN 1601-5223, Vol. 118, no 2, p. 121-130Article in journal (Refereed)
    Abstract [en]

    Many different drugs may be used in selecting cells for multidrug resistance (MDR). Enhanced expression and/or gene amplification is known to cause overproduction of membrane-bound 170,000 P-glycoproteins, responsible for the MDR. In rodents, the P-glycoproteins are encoded by a small gene family: mdr 1a, mdr 1b, and mdr2. To evaluate the relationship between the pattern of MDR and the selecting drug, nine MDR sublines were independently selected from a sensitive mouse tumor cell line, SEWATC13K, using three different drugs. Each MDR subline displayed amplification of one or more of the three mdr genes, but only one, mdr 1a, was consistently overexpressed. Thus, our results indicate that the pattern of mdr gene amplification and overexpression is independent of the selective agent. Furthermore, in four of the MDR sublines, where all three mdr genes had been originally amplified, pulsed field gel electrophoresis (PFGE) revealed that amplification of mdr 1a, only, was a second step of gene amplification. In addition, the gene for the calcium-binding protein, sorcin, was coamplified in eight of the nine MDR sublines. The sorcin gene was overexpressed in seven of these eight sublines. Finally, hybridizations with a probe homologous with a putative region of RFLP (restriction fragment length polymorphism), indicated that the amplified sequences originate from one or the other of the two homologous chromosomes with no preference.

  • 55. Ståhl, Fredrik
    et al.
    Wettergren, Y
    Levan, G
    OFAGE analysis of large DNA restriction fragments from multidrug resistant SEWA mouse cells1990In: Hereditas, Wiley-Blackwell Publishing, Inc. , 1990, p. 9-Conference paper (Refereed)
    Abstract [en]

    The aim of this study is to detect similarities and differences in the gene amplification process, when MDR cells develop after selection in different drugs. For this purpose, nine independent MDR sublines of the murine SEWA TC13K cell line were established by stepwise selection in actinomycinD( Al,A2,A4),colcemid(Cl,C2,C3),or vincristine (Vl, V3, V4). All MDR sublines displayed numerous DMs. DNA from all lines was digested with EcoRl and the infrequently cutting enzyme SfiI. DNA-fragments from the SfiI-digests were separated by orthogonal field alterating gel electrophoresis (OFAGE). Hybridizations were made with two probes: (1) cp28, a Chinese hamster P-glycoprotein cDNA sequence, kindly supplied by Dr Alexander Van der Bliek, The Netherlands Cancer Institute in Amsterdam; (2) Ie7, a genomic clone from a DM mini-library (Stihl et al., Hereditas 106:97, 1987). The hybridization patterns of the Sfildigests were very similar for both probes, while the patterns of the EcoRI-digests differed considerably. No drugspecific amplification pattern was revealed. The Ie7 probe did not cross-hybridize to the cp28 cDNA-sequence. However, low stringency hybridization of Ie7 to a 4.5 kb mRNA (hamster) has been reported (Diddens et al., Int. J. Cancer 40:635, 1987). Still, the similarities in the hybridization patterns suggest that Ie7 DNA-sequence is located close to the cp28 DNA-sequence, perhaps as a part of an intron. In the SfiI digest the cp28 probe hybridized to seven DNA-fragments (six of which were detected also with Ie7) that were amplified in most of the lines. The same DNAfragments were present but not amplified in the control line TC13K. The presence of several hybridizing fragments also in the control line is probably due to homology within the P-glycoprotein gene family. Other amplified sequences were unique to each cell line and are presumably a result of so-called novel joints. The large number of new hybridizing fragments thus reflects a recombinational process during amplicon formation. The presence of specific cytogenetic markers in some of the cell lines indicated that the MDR cells were of monoclonal origin. Therefore, it is possible that each line contains a homogeneous population of DMs, each contributing the same complex pattern of novel fragments in the SfiI analysis. Another explanation of this complexity would be thai different amplicons (with different novel joints) are located on different DMs in a heterogeneous DM population.

  • 56. Szpirer, C
    et al.
    Szpirer, J
    Klinga-Levan, K
    Ståhl, Fredrik
    University of Borås, School of Health Science.
    Levan, G
    The rat: an experimental animal in serach of a genetic map1996In: Folia biologica (Praha), ISSN 0015-5500, Vol. 42, no 4, p. 175-226Article in journal (Refereed)
  • 57. Twigger, S
    et al.
    Lu, J
    Shimoyama, M
    Pasko, D
    Long, P
    Ginster, J
    Chen, CF
    Nigam, R
    Chen, D
    Wang, Z
    Kwitek-Black, A
    Eppig, J
    Maglott, D
    Schuler, G
    Ståhl, Fredrik
    Levan, G
    Jacob, H
    Tonellato, J
    Rat Genome Database: A comparative genomics platform for rat mouse and human.2001In: Journal of Molecular Medicine, Springer , 2001, p. B30-Conference paper (Refereed)
    Abstract [en]

    The Rat Genome Database (RGD) is a NIH funded project who’s stated mission is “to collect, consolidate, and integrate data generated from ongoing rat genetic and genomic research efforts and make these data widely available to the scientific community.” In a collaboration between the Medical College of Wisconsin, the Jackson Lab, the National Center for Biotechnology and Information and the Genetics Lundberg Laboratory, Gothenburg, Sweden, RGD has been created to meet these stated aims. The primary focus of RGD is to aid Rat researchers in their work studying the rat as a model organism for human disease. To support these studies we have integrated a large amount of rat genetic and genomic resources in RGD and these are constantly being expanded through ongoing literature curation. One of the major features of RGD version 1.1, released in January of this year, is incorporation of QTL data to facilitate physiological genomics studies relating disease with the genome. In addition, a dynamic sequence-based homology tool is in final testing which will enable Rat, Mouse and Human researchers to view mapped genes and sequences and their locations in the other two organisms. We hope to release this tool in the second quarter of 2001. This will facilitate the application of results in one species to experiments in another species. In collaboration with the Mouse Genome Database and NCBI, close links are being created between RGD and MGD, LocusLink and UniGene to increase access to each set of data. To support its other general functions RGD has a variety of tools available for the rat researcher, plus ones that are equally useful to researchers working in other organisms and a sampling of these tools will be presented. Thus RGD is not only a valuable resource for those working with the rat but also for researchers in other model organisms wishing to harness the existing genetic and physiological data available in the rat to complement their own work.

  • 58. van Zutphen, L. F. M
    et al.
    den Bieman, M
    Ståhl, Fredrik
    van Lith, H.A
    Report on rat chromosome 6.1998Report (Other academic)
  • 59. van Zutphen, LFM
    et al.
    den Bieman, M
    Ståhl, Fredrik
    van Lith, HA
    Report on rat chromosome 61999Report (Other academic)
  • 60. Yamasaki, Y
    et al.
    Helou, K
    Watanabw, TK
    Sjöling, Å
    Suzuki, M
    Okuno, S
    Ono, T
    Takagi, T
    Nakamura, Y
    Ståhl, Fredrik
    Tanigami, A
    Mouse Chromosome 19 and Distal Rat Chromosome 1: a Chromosome Segment Conserved in Evolution2001In: Hereditas, ISSN 0018-0661, E-ISSN 1601-5223, Vol. 134, no 1, p. 23-34Article in journal (Refereed)
    Abstract [en]

    Through a combination of radiation hybrid mapping and studies by FISH and zoo-FISH we have made a comparative investigation of the distal portion of rat chromosome 1 (RNO1) and the entire mouse chromosome 19(MMU19). It was found that homologous segments of RNO1 and MMU19 are similar in banding morphology and in length as determined by several different methods, and that the gene order of the 46 genes studied appears to be conserved across the homologous segments in the two species. High-resolution zoo-FISH techniques showed that MMU19 probes highlight only a continuous segment on RNO1 (Iq43-qter), with no detectable signals on other rat chromosomes. We conclude that these data suggest the evolutionary conservation of a chromosomal segment from a common rodent ancestor. This segment now constitutes the entire MMU19 and a large segment distally on RNO1q in the mouse and rat, respectively.

12 51 - 60 of 60
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • harvard-cite-them-right
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf