The Role of Arrestins in Visual and Disease Processes of the Eye - Progress in Molecular Biology and Translational Science - page 236

1. VISUAL ARRESTIN NOMENCLATURE

It is always a good idea to begin any discussion with a clear under-
standing of the vocabulary being used. Because the visual arrestins were dis-
covered independently by laboratories that were studying different
processes, there has been a proliferation of arrestin synonyms. For example,
immunologists focusing on the immunogenic properties of arrestin referred
to arrestin as “soluble antigen,” or “S-antigen,” owing to arrestin's ability to
induce autoimmune uveoretinitis. 1,2 Physiologists studying the function of
an abundant retinal protein called it the “48-kDa protein”, based on its
apparent molecular mass measured by gel electrophoresis. 3 In both cases,
the same protein was being studied and was proved to be the first member
of what has become the arrestin family. 4,5 This protein is now designated as
arrestin1, the abundant retinal arrestin principally localized in rod photore-
ceptors, and thus has been variously indicated in the literature as rod arrestin,
visual arrestin, S-antigen, and 48-kDa protein. Similarly, arrestin4 was orig-
inally identified as being expressed in pinealocytes and cone photoreceptors
and is variously known as cone arrestin 6,7 or X-arrestin, because of
its genetic localization to the X chromosome. 8,9 To maintain clarity in this
chapter, we use the more widely accepted designation of these members of
the arrestin family as arrestin1 and arrestin4, occasionally referring to the
aggregate of the two proteins as the visual arrestins, owing to their nearly
exclusive expression in visual tissues.

2. THE FUNCTION OF VISUAL ARRESTINS IN QUENCHING
PHOTOTRANSDUCTION

Much of what is known about arrestin function in visual signaling was
learned in retinal photoreceptors, owing to the natural concentration of
visual pigments and associated components. Phototransduction, the process
of converting the energy of a photon into a change in membrane potential
that can be synaptically transmitted to the brain, begins with the absorption
of light by the 11- cis retinoid chromophore of rhodopsin. In this canonical
G-protein-coupled receptor, changes in the configuration of the retinoid to
all- trans induces conformational changes in rhodopsin that allow the activa-
tion of the guanine nucleotide-binding protein, transducin, and the activa-
tion of the subsequent phototransduction cascade components that