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  • 1.
    Ståhl, Fredrik
    et al.
    Högskolan i Borås, Akademin för vård, arbetsliv och välfärd.
    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 cells1988Ingår i: Hereditas, ISSN 0018-0661, E-ISSN 1601-5223, Vol. 108, nr 2, s. 251-258Artikel i tidskrift (Refereegranskat)
  • 2.
    Ståhl, Fredrik
    et al.
    Högskolan i Borås, Akademin för vård, arbetsliv och välfärd.
    Sandberg, P
    Martinsson, T
    Skoog, J
    Dahllöf, B
    Wettergren, Y
    Bjursell, G
    Levan, G
    Isolation of selectively amplified DNA sequences from multidrug-resistant SEWA cells1987Ingår i: Hereditas, ISSN 0018-0661, E-ISSN 1601-5223, Vol. 106, nr 1, s. 97-105Artikel i tidskrift (Refereegranskat)
  • 3. 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 lines1993Ingår i: Hereditas, ISSN 0018-0661, E-ISSN 1601-5223, Vol. 118, nr 2, s. 121-130Artikel i tidskrift (Refereegranskat)
    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.

  • 4. 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 Evolution2001Ingår i: Hereditas, ISSN 0018-0661, E-ISSN 1601-5223, Vol. 134, nr 1, s. 23-34Artikel i tidskrift (Refereegranskat)
    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.

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