RGD Reference Report - Developmental expression of dysbindin in Muller cells of rat retina. - Rat Genome Database

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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.
RGD ID: 11251759
Pubmed: PMID:23954924   (View Abstract at PubMed)
DOI: DOI:10.1016/j.exer.2013.08.006   (Journal Full-text)

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.



Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Dtnbp1Ratretina development in camera-type eye  IEP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Dtnbp1  (dystrobrevin binding protein 1)


Additional Information