Effects of Mercury on Ras/MAP Kinase Signaling in T Cells
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Authors
Felczak, Aimee M.
Issue Date
2001
Type
Thesis
Language
en_US
Keywords
Alternative Title
Abstract
A major task of the immune system is to distinguish self from non-self. Usually
the self-reacting cells die by apoptosis before they mature, however, failure of this
process results in autoimmune abnormalities. The molecular cause of autoimmunity is
unknown. It is proposed that genetic predisposition and environmental toxins both
increase susceptibility toward autoimmune diseases. Studies indicate that mercury is a
causal agent in autoimmune diseases. In lymphocytes, mercury is suggested to interfere with the apoptotic cell death signaling pathway. Studies demonstrate that mercury induces protein tyrosine phosphorylation, which may be linked to the initiation of
intracellular phosphorylation cascades. We hypothesize that mercury interferes with the
functioning of the Ras/MAP kinase cell survival pathway, a well-known phosphorylation
cascade. To test our hypothesis we performed cell culture experiments evaluating the
level of protein activation induced by cell surface receptor stimulating reagents in the
presence and absence of mercury. The results from our study indicate that low
concentrations (<10 µM) of mercury weakly activate Ras by receptor stimulation.
However, mercury had no effect on MAP kinase, a downstream protein of Ras. Thus,
inorganic mercury interferes with the completion of Ras/MAP kinase survival pathway,
which may play a role in the disregulation of other cell signaling cascades.
Description
v, 55 p.
Citation
Publisher
Kalamazoo College
License
U.S. copyright laws protect this material. Commercial use or distribution of this material is not permitted without prior written permission of the copyright holder.