The Experts below are selected from a list of 60 Experts worldwide ranked by ideXlab platform

Leena Alhonen - One of the best experts on this subject based on the ideXlab platform.

  • Regulation of the expression of human Ornithine Decarboxylase gene and Ornithine Decarboxylase promoter-driven reporter gene in transgenic mice.
    Biochemical Journal, 1993
    Co-Authors: Maria Halmekytö, Juha-matti Hyttinen, Riitta Sinervirta, Pia Leppänen, Juhani Jänne, Leena Alhonen
    Abstract:

    We have studied the regulation of the expression of Ornithine Decarboxylase with the aid of transgenic mice harbouring either functional human Ornithine Decarboxylase genes or the mouse Ornithine Decarboxylase promoter-driven chloramphenicol acetyltransferase fusion gene in their genome. We used three different stimuli which are well known to enhance Ornithine Decarboxylase activity in their appropriate target tissues: (i) testosterone in female kidney, (ii) a phorbol ester in epidermis and (iii) partial hepatectomy in liver. Endogenous mouse Ornithine Decarboxylase activity was strikingly stimulated in response to these treatments. Even though containing the 5' flanking region of the mouse Ornithine Decarboxylase gene, known to possess full promoter activity, the chloramphenicol acetyltransferase reporter gene was entirely insensitive to any of these stimuli. The human transgene-derived Ornithine Decarboxylase activity in kidney was unaffected by testosterone treatment, but responded in skin to application of the phorbol ester and likewise was clearly enhanced in regenerating liver. Although mouse endogenous Ornithine Decarboxylase mRNA levels were distinctly elevated after testosterone, this treatment did not influence the accumulation of the human transgene-derived mRNA. The phorbol ester enhanced the accumulation of mouse endogenous Ornithine Decarboxylase mRNA and also that derived from the human transgene; however, the enzyme activity was stimulated in regenerating liver without appreciable changes in the levels of endogenous or transgene-derived message. Our present results strongly emphasize the central role of the coding sequence or Ornithine Decarboxylase gene in the induction of the enzyme activity.

  • Transgenic mice aberrantly expressing human Ornithine Decarboxylase gene.
    The Journal of biological chemistry, 1991
    Co-Authors: Maria Halmekytö, Juha-matti Hyttinen, Riitta Sinervirta, M Utriainen, S Myöhänen, H M Voipio, Jarmo Wahlfors, S Syrjänen, K Syrjänen, Leena Alhonen
    Abstract:

    Abstract We have generated transgenic mice carrying human Ornithine Decarboxylase gene. Two different transgene constructs were used: (i) a 5'-truncated human Ornithine Decarboxylase gene and (ii) an intact human Ornithine Decarboxylase gene. Transgenic mice carrying the 5'-truncated gene did not express human Ornithine Decarboxylase-specific mRNA. Transgenic mice carrying the intact human Ornithine Decarboxylase gene expressed human-specific Ornithine Decarboxylase mRNA in all tissues studied. However, as indicated by actual enzyme assays, the expression pattern was highly unusual. In comparison with their wild-type littermates, the transgenic mice exhibited greatly elevated enzyme activity in almost every tissue studied. Ornithine Decarboxylase activity was moderately elevated in parenchymal organs such as liver, kidney, and spleen. Tissues like heart, muscle, lung, thymus, testis, and brain displayed an enzyme activity that was 20 to 80 times higher than that in the respective tissues of nontransgenic animals. The offspring of the first transgenic male founder animal did not show any overt abnormalities, yet their reproductive performance was reduced. The second transgenic founder animal, showing similar aberrant expression of Ornithine Decarboxylase in all tissues studied, including an extremely high activity in testis, was found to be infertile. Histological examination of the tissues of the latter animal revealed marked changes in testicular morphology. The germinal epithelium was hypoplastic, and the spermatogenesis was virtually totally shut off. Similar examination of male members of the first transgenic mouse line revealed comparable, yet less severe, histological changes in testis.

Maria Halmekytö - One of the best experts on this subject based on the ideXlab platform.

  • Regulation of the expression of human Ornithine Decarboxylase gene and Ornithine Decarboxylase promoter-driven reporter gene in transgenic mice.
    Biochemical Journal, 1993
    Co-Authors: Maria Halmekytö, Juha-matti Hyttinen, Riitta Sinervirta, Pia Leppänen, Juhani Jänne, Leena Alhonen
    Abstract:

    We have studied the regulation of the expression of Ornithine Decarboxylase with the aid of transgenic mice harbouring either functional human Ornithine Decarboxylase genes or the mouse Ornithine Decarboxylase promoter-driven chloramphenicol acetyltransferase fusion gene in their genome. We used three different stimuli which are well known to enhance Ornithine Decarboxylase activity in their appropriate target tissues: (i) testosterone in female kidney, (ii) a phorbol ester in epidermis and (iii) partial hepatectomy in liver. Endogenous mouse Ornithine Decarboxylase activity was strikingly stimulated in response to these treatments. Even though containing the 5' flanking region of the mouse Ornithine Decarboxylase gene, known to possess full promoter activity, the chloramphenicol acetyltransferase reporter gene was entirely insensitive to any of these stimuli. The human transgene-derived Ornithine Decarboxylase activity in kidney was unaffected by testosterone treatment, but responded in skin to application of the phorbol ester and likewise was clearly enhanced in regenerating liver. Although mouse endogenous Ornithine Decarboxylase mRNA levels were distinctly elevated after testosterone, this treatment did not influence the accumulation of the human transgene-derived mRNA. The phorbol ester enhanced the accumulation of mouse endogenous Ornithine Decarboxylase mRNA and also that derived from the human transgene; however, the enzyme activity was stimulated in regenerating liver without appreciable changes in the levels of endogenous or transgene-derived message. Our present results strongly emphasize the central role of the coding sequence or Ornithine Decarboxylase gene in the induction of the enzyme activity.

  • Transgenic mice aberrantly expressing human Ornithine Decarboxylase gene.
    The Journal of biological chemistry, 1991
    Co-Authors: Maria Halmekytö, Juha-matti Hyttinen, Riitta Sinervirta, M Utriainen, S Myöhänen, H M Voipio, Jarmo Wahlfors, S Syrjänen, K Syrjänen, Leena Alhonen
    Abstract:

    Abstract We have generated transgenic mice carrying human Ornithine Decarboxylase gene. Two different transgene constructs were used: (i) a 5'-truncated human Ornithine Decarboxylase gene and (ii) an intact human Ornithine Decarboxylase gene. Transgenic mice carrying the 5'-truncated gene did not express human Ornithine Decarboxylase-specific mRNA. Transgenic mice carrying the intact human Ornithine Decarboxylase gene expressed human-specific Ornithine Decarboxylase mRNA in all tissues studied. However, as indicated by actual enzyme assays, the expression pattern was highly unusual. In comparison with their wild-type littermates, the transgenic mice exhibited greatly elevated enzyme activity in almost every tissue studied. Ornithine Decarboxylase activity was moderately elevated in parenchymal organs such as liver, kidney, and spleen. Tissues like heart, muscle, lung, thymus, testis, and brain displayed an enzyme activity that was 20 to 80 times higher than that in the respective tissues of nontransgenic animals. The offspring of the first transgenic male founder animal did not show any overt abnormalities, yet their reproductive performance was reduced. The second transgenic founder animal, showing similar aberrant expression of Ornithine Decarboxylase in all tissues studied, including an extremely high activity in testis, was found to be infertile. Histological examination of the tissues of the latter animal revealed marked changes in testicular morphology. The germinal epithelium was hypoplastic, and the spermatogenesis was virtually totally shut off. Similar examination of male members of the first transgenic mouse line revealed comparable, yet less severe, histological changes in testis.

Riitta Sinervirta - One of the best experts on this subject based on the ideXlab platform.

  • Regulation of the expression of human Ornithine Decarboxylase gene and Ornithine Decarboxylase promoter-driven reporter gene in transgenic mice.
    Biochemical Journal, 1993
    Co-Authors: Maria Halmekytö, Juha-matti Hyttinen, Riitta Sinervirta, Pia Leppänen, Juhani Jänne, Leena Alhonen
    Abstract:

    We have studied the regulation of the expression of Ornithine Decarboxylase with the aid of transgenic mice harbouring either functional human Ornithine Decarboxylase genes or the mouse Ornithine Decarboxylase promoter-driven chloramphenicol acetyltransferase fusion gene in their genome. We used three different stimuli which are well known to enhance Ornithine Decarboxylase activity in their appropriate target tissues: (i) testosterone in female kidney, (ii) a phorbol ester in epidermis and (iii) partial hepatectomy in liver. Endogenous mouse Ornithine Decarboxylase activity was strikingly stimulated in response to these treatments. Even though containing the 5' flanking region of the mouse Ornithine Decarboxylase gene, known to possess full promoter activity, the chloramphenicol acetyltransferase reporter gene was entirely insensitive to any of these stimuli. The human transgene-derived Ornithine Decarboxylase activity in kidney was unaffected by testosterone treatment, but responded in skin to application of the phorbol ester and likewise was clearly enhanced in regenerating liver. Although mouse endogenous Ornithine Decarboxylase mRNA levels were distinctly elevated after testosterone, this treatment did not influence the accumulation of the human transgene-derived mRNA. The phorbol ester enhanced the accumulation of mouse endogenous Ornithine Decarboxylase mRNA and also that derived from the human transgene; however, the enzyme activity was stimulated in regenerating liver without appreciable changes in the levels of endogenous or transgene-derived message. Our present results strongly emphasize the central role of the coding sequence or Ornithine Decarboxylase gene in the induction of the enzyme activity.

  • Transgenic mice aberrantly expressing human Ornithine Decarboxylase gene.
    The Journal of biological chemistry, 1991
    Co-Authors: Maria Halmekytö, Juha-matti Hyttinen, Riitta Sinervirta, M Utriainen, S Myöhänen, H M Voipio, Jarmo Wahlfors, S Syrjänen, K Syrjänen, Leena Alhonen
    Abstract:

    Abstract We have generated transgenic mice carrying human Ornithine Decarboxylase gene. Two different transgene constructs were used: (i) a 5'-truncated human Ornithine Decarboxylase gene and (ii) an intact human Ornithine Decarboxylase gene. Transgenic mice carrying the 5'-truncated gene did not express human Ornithine Decarboxylase-specific mRNA. Transgenic mice carrying the intact human Ornithine Decarboxylase gene expressed human-specific Ornithine Decarboxylase mRNA in all tissues studied. However, as indicated by actual enzyme assays, the expression pattern was highly unusual. In comparison with their wild-type littermates, the transgenic mice exhibited greatly elevated enzyme activity in almost every tissue studied. Ornithine Decarboxylase activity was moderately elevated in parenchymal organs such as liver, kidney, and spleen. Tissues like heart, muscle, lung, thymus, testis, and brain displayed an enzyme activity that was 20 to 80 times higher than that in the respective tissues of nontransgenic animals. The offspring of the first transgenic male founder animal did not show any overt abnormalities, yet their reproductive performance was reduced. The second transgenic founder animal, showing similar aberrant expression of Ornithine Decarboxylase in all tissues studied, including an extremely high activity in testis, was found to be infertile. Histological examination of the tissues of the latter animal revealed marked changes in testicular morphology. The germinal epithelium was hypoplastic, and the spermatogenesis was virtually totally shut off. Similar examination of male members of the first transgenic mouse line revealed comparable, yet less severe, histological changes in testis.

Juha-matti Hyttinen - One of the best experts on this subject based on the ideXlab platform.

  • Regulation of the expression of human Ornithine Decarboxylase gene and Ornithine Decarboxylase promoter-driven reporter gene in transgenic mice.
    Biochemical Journal, 1993
    Co-Authors: Maria Halmekytö, Juha-matti Hyttinen, Riitta Sinervirta, Pia Leppänen, Juhani Jänne, Leena Alhonen
    Abstract:

    We have studied the regulation of the expression of Ornithine Decarboxylase with the aid of transgenic mice harbouring either functional human Ornithine Decarboxylase genes or the mouse Ornithine Decarboxylase promoter-driven chloramphenicol acetyltransferase fusion gene in their genome. We used three different stimuli which are well known to enhance Ornithine Decarboxylase activity in their appropriate target tissues: (i) testosterone in female kidney, (ii) a phorbol ester in epidermis and (iii) partial hepatectomy in liver. Endogenous mouse Ornithine Decarboxylase activity was strikingly stimulated in response to these treatments. Even though containing the 5' flanking region of the mouse Ornithine Decarboxylase gene, known to possess full promoter activity, the chloramphenicol acetyltransferase reporter gene was entirely insensitive to any of these stimuli. The human transgene-derived Ornithine Decarboxylase activity in kidney was unaffected by testosterone treatment, but responded in skin to application of the phorbol ester and likewise was clearly enhanced in regenerating liver. Although mouse endogenous Ornithine Decarboxylase mRNA levels were distinctly elevated after testosterone, this treatment did not influence the accumulation of the human transgene-derived mRNA. The phorbol ester enhanced the accumulation of mouse endogenous Ornithine Decarboxylase mRNA and also that derived from the human transgene; however, the enzyme activity was stimulated in regenerating liver without appreciable changes in the levels of endogenous or transgene-derived message. Our present results strongly emphasize the central role of the coding sequence or Ornithine Decarboxylase gene in the induction of the enzyme activity.

  • Transgenic mice aberrantly expressing human Ornithine Decarboxylase gene.
    The Journal of biological chemistry, 1991
    Co-Authors: Maria Halmekytö, Juha-matti Hyttinen, Riitta Sinervirta, M Utriainen, S Myöhänen, H M Voipio, Jarmo Wahlfors, S Syrjänen, K Syrjänen, Leena Alhonen
    Abstract:

    Abstract We have generated transgenic mice carrying human Ornithine Decarboxylase gene. Two different transgene constructs were used: (i) a 5'-truncated human Ornithine Decarboxylase gene and (ii) an intact human Ornithine Decarboxylase gene. Transgenic mice carrying the 5'-truncated gene did not express human Ornithine Decarboxylase-specific mRNA. Transgenic mice carrying the intact human Ornithine Decarboxylase gene expressed human-specific Ornithine Decarboxylase mRNA in all tissues studied. However, as indicated by actual enzyme assays, the expression pattern was highly unusual. In comparison with their wild-type littermates, the transgenic mice exhibited greatly elevated enzyme activity in almost every tissue studied. Ornithine Decarboxylase activity was moderately elevated in parenchymal organs such as liver, kidney, and spleen. Tissues like heart, muscle, lung, thymus, testis, and brain displayed an enzyme activity that was 20 to 80 times higher than that in the respective tissues of nontransgenic animals. The offspring of the first transgenic male founder animal did not show any overt abnormalities, yet their reproductive performance was reduced. The second transgenic founder animal, showing similar aberrant expression of Ornithine Decarboxylase in all tissues studied, including an extremely high activity in testis, was found to be infertile. Histological examination of the tissues of the latter animal revealed marked changes in testicular morphology. The germinal epithelium was hypoplastic, and the spermatogenesis was virtually totally shut off. Similar examination of male members of the first transgenic mouse line revealed comparable, yet less severe, histological changes in testis.

Rentala Madhubala - One of the best experts on this subject based on the ideXlab platform.

  • Leishmania donovani: cellular control of Ornithine Decarboxylase in promastigotes.
    The international journal of biochemistry & cell biology, 1995
    Co-Authors: Rita Mukhopadhyay, Rentala Madhubala
    Abstract:

    Ornithine Decarboxylase, a key enzyme in polyamine biosynthesis, is essential for normal cell growth and proliferation. Furthermore, the inhibition of this enzyme is a potential way of controlling such growth. In order to shed light on the role of Ornithine Decarboxylase in regulation of Leishmania growth we examined the activity of this enzyme during the life cycle of these organisms. Exponentially growing Leishmania promastigotes were resuspended at a density of 3 x 10(6) cells/ml. 2 x 10(7) cells were withdrawn 24 hr later at different time intervals for induction studies and Ornithine Decarboxylase activity was measured. Ornithine Decarboxylase showed a growth related pattern in L. donovani promastigotes. Induction studies showed that Ornithine Decarboxylase activity rapidly increased in late log phase cells when resuspended in fresh medium. A biphasic induction curve was observed similar to that observed in mammalian cells. The first peak was observed at 6 hr and the second at 16 hr. Cycloheximide and Actinomycin D inhibited induction at 16 hr by 65-68%. Polyamines at a level not inhibitory to growth (10 microM) inhibited Ornithine Decarboxylase induction by 30-40% late in the induction period. Putrescine and spermidine both inhibited the first peak of induction. Putrescine suppressed Ornithine Decarboxylase activity by 39% at 16 hr whereas spermidine by only 29%. The half life of Ornithine Decarboxylase in promastigote forms grown in the presence of cycloheximide was >6 hr. These studies indicate that although the Leishmanial Ornithine Decarboxylase follows a similar induction pattern to that previously reported in the mammalian cells, it is less susceptible to exogenous polyamines and is comparatively stable. This lack of Ornithine Decarboxylase regulation and turnover may be exploitable in the development of various therapeutic agents to inhibit Leishmanial growth.