Bestrophin proteins in ocular epithelial cells - By: Brooke Pens

Although infection induced sight defects have deteriorated markedly in the Western world, blindness due to other causes has increased dramatically. As well as diseases like diabetes, there are a range of visual conditions caused by mutation or disruptions in the protein pathways controlling sight. The Bestrophin family – in particular, Bestrophin 1 – have been the subject of several antibody studies.

There are four members of the Bestrophin family, of which two – BEST1 and BEST2 – are expressed in the eye. The BEST1 gene (formerly known as VMD2), was identified in 1998, and is of great interest owing to the wide number of mutations it is susceptible to – more than 120 have been catalogued. Four serious eye diseases have been clinically identified, and researchers have run numerous BEST1 antibody studies to examine how mutations in the gene can lead to such uniquely presented diseases. The majority of studies have concentrated on the most common of the four conditions, BVMD (best vitelliform macular dystrophy).

BVMD is an early-onset macular degenerative disease, characterised by a decreased electrooculogram light peak. BEST1 is localised at the basolateral plasma membrane of the epithelium of the retinal pigment. It acts as a Calcium-activated Chloride channel (CaCC), pointing to a function in the production of aqueous humour (AH). Data from various antibody studies initially suggested that BEST1 was responsible for the ECO light peak. However, more recent BEST1 murine studies, plus the discovery of a new, recessive bestrophin disease, suggest otherwise.

The majority of bestrophin products in commercial antibody catalogues are targeted to BEST1. In 2009, interest switched to BEST2, following the discovery that it is expressed in non-pigmented epithelial cells in the ciliary body. The hypothesis was that BEST2 is a Chloride channel necessary for the formation of aqueous humor. However, the results showed that BEST2 antagonised its formation. Disruption of the BEST2 protein led to decreased ocular pressure, showing it may have a role to play in glaucoma therapy.
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