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Developmental expression of dysbindin in Muller cells of rat retina.

Authors: Matteucci, A  Gaddini, L  Macchia, G  Varano, M  Petrucci, TC  Macioce, P  Malchiodi-Albedi, F  Ceccarini, M 
Citation: Matteucci A, etal., Exp Eye Res. 2013 Nov;116:1-8. doi: 10.1016/j.exer.2013.08.006. Epub 2013 Aug 14.
Pubmed: (View Article at PubMed) PMID:23954924
DOI: Full-text: DOI:10.1016/j.exer.2013.08.006

Dysbindin, the product of the DTNBP1 gene, was identified by yeast two hybrid assay as a binding partner of dystrobrevin, a cytosolic component of the dystrophin protein complex. Although its functional role has not yet been completely elucidated, the finding that dysbindin assembles into the biogenesis of lysosome related organelles complex 1 (BLOC-1) suggests that it participates in intracellular trafficking and biogenesis of organelles and vesicles. Dysbindin is ubiquitous and in brain is expressed primarily in neurons. Variations at the dysbindin gene have been associated with increased risk for schizophrenia. As anomalies in retinal function have been reported in patients suffering from neuropsychiatric disorders, we investigated the expression of dysbindin in the retina. Our results show that differentially regulated dysbindin isoforms are expressed in rat retina during postnatal maturation. Interestingly, we found that dysbindin is mainly localized in Muller cells. The identification of dysbindin in glial cells may open new perspectives for a better understanding of the functional involvement of this protein in visual alterations associated to neuropsychiatric disorders.

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CRRD Object Information
CRRD ID: 11251759
Created: 2016-06-21
Species: All species
Last Modified: 2016-06-21
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.