The Experts below are selected from a list of 84156 Experts worldwide ranked by ideXlab platform
John W Commissiong - One of the best experts on this subject based on the ideXlab platform.
-
oligodendrocyte type 2 astrocyte o 2a progenitors increase the survival of rat mesencephalic dopaminergic neurons from death induced by serum deprivation
Neuroscience Letters, 1994Co-Authors: Takao Takeshima, Jane M Johnston, John W CommissiongAbstract:Abstract When a primary culture of E16 rat striatal cells was grown in a serum-free medium, treatment with basic fibroblast growth Factor (bFGF, 10 ng/ml) caused the generation of the progenitor cell for oligodendrocytes and type-2 astrocytes (O-2A). Immunostaining tests confirmed that > 90% of the cells were positive for A2B5, and + ) neurons increased 23-fold and 668-fold at the 5th and 10th days, respectively, compared with control cultures plated on poly- d -lysine. Conditioned medium from the O-2A progenitor cultures also decreased the death of TH + neurons. The mitotic inhibitor, cytosine arabinoside (1.0 μM), did not block the protective effect of the O-2A progenitor cells. O-2A progenitor cells produce a potent, Soluble Factor, that mediates the increased survival of dopaminergic neurons in vitro.
James Burns - One of the best experts on this subject based on the ideXlab platform.
-
modulation of immune system function by measles virus infection role of Soluble Factor and direct infection
Journal of Virology, 1998Co-Authors: Robert S. Fujinami, Joseph M Howell, James C Jenkin, James BurnsAbstract:Measles virus infection can result in a variety of immunologic defects. We have begun studies to determine the basis for the lack of immune responsiveness to antigen and mitogen following infection. Here we present data showing that Epstein-Barr virus-transformed B-cell lines infected with measles virus produce a Soluble Factor that can inhibit antigen-specific T-cell proliferation and inhibit the proliferation of uninfected B cells. The Soluble Factor was neither interleukin-10, transforming growth Factor β, nor alpha/beta interferon. B cells infected with measles virus or treated with the Soluble Factor were unable to present antigen to T cells in a manner that supported antigen-specific proliferation. This could represent one mechanism of how measles virus limits T-cell expansion. However, we found that once CD4+ or CD8+ T cells were activated, their cytolytic activity was intact whether infected with measles virus or treated with Soluble Factor. Thus, while slow to be generated these cytoxic cells could participate in viral clearance.
Takao Takeshima - One of the best experts on this subject based on the ideXlab platform.
-
oligodendrocyte type 2 astrocyte o 2a progenitors increase the survival of rat mesencephalic dopaminergic neurons from death induced by serum deprivation
Neuroscience Letters, 1994Co-Authors: Takao Takeshima, Jane M Johnston, John W CommissiongAbstract:Abstract When a primary culture of E16 rat striatal cells was grown in a serum-free medium, treatment with basic fibroblast growth Factor (bFGF, 10 ng/ml) caused the generation of the progenitor cell for oligodendrocytes and type-2 astrocytes (O-2A). Immunostaining tests confirmed that > 90% of the cells were positive for A2B5, and + ) neurons increased 23-fold and 668-fold at the 5th and 10th days, respectively, compared with control cultures plated on poly- d -lysine. Conditioned medium from the O-2A progenitor cultures also decreased the death of TH + neurons. The mitotic inhibitor, cytosine arabinoside (1.0 μM), did not block the protective effect of the O-2A progenitor cells. O-2A progenitor cells produce a potent, Soluble Factor, that mediates the increased survival of dopaminergic neurons in vitro.
Robert S. Fujinami - One of the best experts on this subject based on the ideXlab platform.
-
modulation of immune system function by measles virus infection role of Soluble Factor and direct infection
Journal of Virology, 1998Co-Authors: Robert S. Fujinami, Joseph M Howell, James C Jenkin, James BurnsAbstract:Measles virus infection can result in a variety of immunologic defects. We have begun studies to determine the basis for the lack of immune responsiveness to antigen and mitogen following infection. Here we present data showing that Epstein-Barr virus-transformed B-cell lines infected with measles virus produce a Soluble Factor that can inhibit antigen-specific T-cell proliferation and inhibit the proliferation of uninfected B cells. The Soluble Factor was neither interleukin-10, transforming growth Factor β, nor alpha/beta interferon. B cells infected with measles virus or treated with the Soluble Factor were unable to present antigen to T cells in a manner that supported antigen-specific proliferation. This could represent one mechanism of how measles virus limits T-cell expansion. However, we found that once CD4+ or CD8+ T cells were activated, their cytolytic activity was intact whether infected with measles virus or treated with Soluble Factor. Thus, while slow to be generated these cytoxic cells could participate in viral clearance.
Joan Massagué - One of the best experts on this subject based on the ideXlab platform.
-
cleavage of the membrane precursor for transforming growth Factor alpha is a regulated process
Proceedings of the National Academy of Sciences of the United States of America, 1991Co-Authors: Atanasio Pandiella, Joan MassaguéAbstract:Transforming growth Factor alpha (TGF-alpha) is generated by cleavage of a membrane-anchored precursor protein, proTGF-alpha. ProTGF-alpha is cleaved at a slow rate and accumulates on the cell surface, thereby mediating cell-cell adhesion and mitogenic stimulation. We show here that cleavage of membrane proTGF-alpha by an elastase-like enzyme constitutes an important regulatory step in the generation of Soluble TGF-alpha. Cleavage is activated in response to serum Factors and tumor-promoting phorbol esters, leading to depletion of cell surface proTGF-alpha, which disperses as Soluble Factor. Activation of proTGF-alpha cleavage is mediated by protein kinase C-dependent and -independent mechanisms. The results demonstrate the existence of mechanisms that control the switch of TGF-alpha from a juxtacrine to a paracrine growth Factor.
