The Experts below are selected from a list of 684 Experts worldwide ranked by ideXlab platform

Jean-marc Gallo - One of the best experts on this subject based on the ideXlab platform.

  • mutually exclusive expression of βiii tubulin and vimentin in Adrenal Cortex Carcinoma sw13 cells
    FEBS Letters, 2000
    Co-Authors: Rachel Butler, Janice Robertson, Jean-marc Gallo
    Abstract:

    During embryogenesis, the maturation of neuroblasts into neurones is accompanied by the down-regulation of vimentin and by the expression of neuronal microtubular proteins. Here, we show that human Adrenal Cortex SW13 cells express βIII-tubulin, MAP2b and tau. Analysis of vimentin-positive and -negative subclones of SW13 cells revealed that, under defined cultured conditions, βIII-tubulin and MAP2b were present only in vimentin-deficient cells and that βIII-tubulin repression occurred at the transcriptional level in vimentin-positive cells. These results suggest that vimentin repression and βIII-tubulin expression are co-ordinated by an upstream mechanism relevant to the control of cytoskeletal protein expression during neuronal development.

  • Mutually exclusive expression of βIII‐tubulin and vimentin in Adrenal Cortex Carcinoma SW13 cells
    FEBS Letters, 2000
    Co-Authors: Rachel Butler, Janice Robertson, Jean-marc Gallo
    Abstract:

    During embryogenesis, the maturation of neuroblasts into neurones is accompanied by the down-regulation of vimentin and by the expression of neuronal microtubular proteins. Here, we show that human Adrenal Cortex SW13 cells express βIII-tubulin, MAP2b and tau. Analysis of vimentin-positive and -negative subclones of SW13 cells revealed that, under defined cultured conditions, βIII-tubulin and MAP2b were present only in vimentin-deficient cells and that βIII-tubulin repression occurred at the transcriptional level in vimentin-positive cells. These results suggest that vimentin repression and βIII-tubulin expression are co-ordinated by an upstream mechanism relevant to the control of cytoskeletal protein expression during neuronal development.

Rachel Butler - One of the best experts on this subject based on the ideXlab platform.

  • mutually exclusive expression of βiii tubulin and vimentin in Adrenal Cortex Carcinoma sw13 cells
    FEBS Letters, 2000
    Co-Authors: Rachel Butler, Janice Robertson, Jean-marc Gallo
    Abstract:

    During embryogenesis, the maturation of neuroblasts into neurones is accompanied by the down-regulation of vimentin and by the expression of neuronal microtubular proteins. Here, we show that human Adrenal Cortex SW13 cells express βIII-tubulin, MAP2b and tau. Analysis of vimentin-positive and -negative subclones of SW13 cells revealed that, under defined cultured conditions, βIII-tubulin and MAP2b were present only in vimentin-deficient cells and that βIII-tubulin repression occurred at the transcriptional level in vimentin-positive cells. These results suggest that vimentin repression and βIII-tubulin expression are co-ordinated by an upstream mechanism relevant to the control of cytoskeletal protein expression during neuronal development.

  • Mutually exclusive expression of βIII‐tubulin and vimentin in Adrenal Cortex Carcinoma SW13 cells
    FEBS Letters, 2000
    Co-Authors: Rachel Butler, Janice Robertson, Jean-marc Gallo
    Abstract:

    During embryogenesis, the maturation of neuroblasts into neurones is accompanied by the down-regulation of vimentin and by the expression of neuronal microtubular proteins. Here, we show that human Adrenal Cortex SW13 cells express βIII-tubulin, MAP2b and tau. Analysis of vimentin-positive and -negative subclones of SW13 cells revealed that, under defined cultured conditions, βIII-tubulin and MAP2b were present only in vimentin-deficient cells and that βIII-tubulin repression occurred at the transcriptional level in vimentin-positive cells. These results suggest that vimentin repression and βIII-tubulin expression are co-ordinated by an upstream mechanism relevant to the control of cytoskeletal protein expression during neuronal development.

Janice Robertson - One of the best experts on this subject based on the ideXlab platform.

  • mutually exclusive expression of βiii tubulin and vimentin in Adrenal Cortex Carcinoma sw13 cells
    FEBS Letters, 2000
    Co-Authors: Rachel Butler, Janice Robertson, Jean-marc Gallo
    Abstract:

    During embryogenesis, the maturation of neuroblasts into neurones is accompanied by the down-regulation of vimentin and by the expression of neuronal microtubular proteins. Here, we show that human Adrenal Cortex SW13 cells express βIII-tubulin, MAP2b and tau. Analysis of vimentin-positive and -negative subclones of SW13 cells revealed that, under defined cultured conditions, βIII-tubulin and MAP2b were present only in vimentin-deficient cells and that βIII-tubulin repression occurred at the transcriptional level in vimentin-positive cells. These results suggest that vimentin repression and βIII-tubulin expression are co-ordinated by an upstream mechanism relevant to the control of cytoskeletal protein expression during neuronal development.

  • Mutually exclusive expression of βIII‐tubulin and vimentin in Adrenal Cortex Carcinoma SW13 cells
    FEBS Letters, 2000
    Co-Authors: Rachel Butler, Janice Robertson, Jean-marc Gallo
    Abstract:

    During embryogenesis, the maturation of neuroblasts into neurones is accompanied by the down-regulation of vimentin and by the expression of neuronal microtubular proteins. Here, we show that human Adrenal Cortex SW13 cells express βIII-tubulin, MAP2b and tau. Analysis of vimentin-positive and -negative subclones of SW13 cells revealed that, under defined cultured conditions, βIII-tubulin and MAP2b were present only in vimentin-deficient cells and that βIII-tubulin repression occurred at the transcriptional level in vimentin-positive cells. These results suggest that vimentin repression and βIII-tubulin expression are co-ordinated by an upstream mechanism relevant to the control of cytoskeletal protein expression during neuronal development.

Anton Wellstein - One of the best experts on this subject based on the ideXlab platform.

  • Autocrine Growth Stimulation by Secreted Kaposi Fibroblast Growth Factor but not by Endogenous Basic Fibroblast Growth Fador’
    2015
    Co-Authors: Anton Wellstein, Ruth Lupu, Gerhard Zugmaier, L Flamm, Andrea L Cheville, Pasquale Delli Bovi, Claudio Basilico, Francis C. Kern
    Abstract:

    We studied the different potentials of a secreted and a nonsecreted member of the fibroblast growth fador (FGF) family to induce autocrine growth stimulation in human Adrenal Cortex Carcinoma cells (SW-13). These epithelial cells express basic FGF (bFGF) cell surface receptors, and picomolar concentrations of bFGF suf-fice to induce anchorage-independent growth. The re-quirement for exogenously added bFGF contrasts with the intracellular storage of biologically adive bFGF in SW-13 cells>10,000-fold in excess of the concentra-tion needed to stimulate anchorage independent growth. To study whether the expression of a secreted FGF would alter the growth phenotype of these cells, we transfeded them with an expression vedor coding for the Kaposi-fgf (K-fgf) oncogene. In contrast to con

  • Autocrine growth stimulation by secreted Kaposi fibroblast growth factor but not by endogenous basic fibroblast growth factor.
    Cell Growth & Differentiation, 1990
    Co-Authors: Anton Wellstein, Ruth Lupu, Gerhard Zugmaier, Andrea L Cheville, Claudio Basilico, S. L. Flamm, P. Delli Bovi, Marc E. Lippman, F. G. Kern
    Abstract:

    We studied the different potentials of a secreted and a nonsecreted member of the fibroblast growth factor (FGF) family to induce autocrine growth stimulation in human Adrenal Cortex Carcinoma cells (SW-13). These epithelial cells express basic FGF (bFGF) cell surface receptors, and picomolar concentrations of bFGF suffice to induce anchorage-independent growth. The requirement for exogenously added bFGF contrasts with the intracellular storage of biologically active bFGF in SW-13 cells greater than 10,000-fold in excess of the concentration needed to stimulate anchorage independent growth. To study whether the expression of a secreted FGF would alter the growth phenotype of these cells, we transfected them with an expression vector coding for the Kaposi-fgf (K-fgf) oncogene. In contrast to controls, K-fgf-transfected cells secrete significant amounts of biologically active K-fgf protein into the growth media, show up to 50-fold increased colony formation in soft agar, and grow into rapidly progressing, highly vascularized tumors in athymic nude mice. A reversible inhibition of the autocrine growth stimulation in vitro is brought about by the polyanionic compound suramin. We conclude that FGF has to be released from SW-13 cells to function fully as a growth stimulator in vitro and in vivo.

F. G. Kern - One of the best experts on this subject based on the ideXlab platform.

  • Autocrine growth stimulation by secreted Kaposi fibroblast growth factor but not by endogenous basic fibroblast growth factor.
    Cell Growth & Differentiation, 1990
    Co-Authors: Anton Wellstein, Ruth Lupu, Gerhard Zugmaier, Andrea L Cheville, Claudio Basilico, S. L. Flamm, P. Delli Bovi, Marc E. Lippman, F. G. Kern
    Abstract:

    We studied the different potentials of a secreted and a nonsecreted member of the fibroblast growth factor (FGF) family to induce autocrine growth stimulation in human Adrenal Cortex Carcinoma cells (SW-13). These epithelial cells express basic FGF (bFGF) cell surface receptors, and picomolar concentrations of bFGF suffice to induce anchorage-independent growth. The requirement for exogenously added bFGF contrasts with the intracellular storage of biologically active bFGF in SW-13 cells greater than 10,000-fold in excess of the concentration needed to stimulate anchorage independent growth. To study whether the expression of a secreted FGF would alter the growth phenotype of these cells, we transfected them with an expression vector coding for the Kaposi-fgf (K-fgf) oncogene. In contrast to controls, K-fgf-transfected cells secrete significant amounts of biologically active K-fgf protein into the growth media, show up to 50-fold increased colony formation in soft agar, and grow into rapidly progressing, highly vascularized tumors in athymic nude mice. A reversible inhibition of the autocrine growth stimulation in vitro is brought about by the polyanionic compound suramin. We conclude that FGF has to be released from SW-13 cells to function fully as a growth stimulator in vitro and in vivo.