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Two sigma receptor subtypes have been proposed, sigma1 and 2. Much
of our understanding of this system is based on biochemical and
pharmacological characterization of the cloned sigma1 receptor
subtype (Sigma1). It has become clear that sigma receptors are not
canonical receptors. Sigma1 is highly conserved among mammalian
species, however, it does not share significant homology with any
other mammalian protein. Although a range of structurally diverse
small molecules bind Sigma1 with high affinity, and it has been
associated with a broad range of signaling systems, Sigma1 itself
has no known signaling or enzymatic activity. The evolution of this
field over nearly four decades has more recently led to a
fundamental shift in the concept of "sigma receptors" to what may
more accurately and generally be called sigma proteins. Largely
based on traditional pharmacologic approaches, the Sigma1 protein
has been associated with a broad range of signaling systems,
including G-protein coupled receptors, NMDA receptors, and ion
channels. Sigma proteins have been linked to a range of
physiological processes, including intracellular calcium signaling,
neuroprotection, learning, memory, and cognition. Emerging genetic,
clinical, and mechanism focused molecular pharmacology data
demonstrate the involvement of proteins in a range of
pathophysiologies and disorders including neurodegenerative
disease, pain, addiction, psychomotor stimulant abuse, and cancer.
However, an understanding of the physiological role of sigma
proteins has remained elusive. Emerging data associate Sigma1 with
chaperone-like activities or molecular scaffold functions. This
book aims to provide an updated perspective on this rapidly
evolving field undergoing changes in fundamental concepts of key
importance to the discipline of pharmacology. It focusses on the
reported roles of sigma proteins in pathophysiology and on emergent
therapeutic initiatives.
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