Abstract:
:There is growing interest in the biology of dysbindin and its genetic locus (DTNBP1) due to genetic variants associated with an increased risk of schizophrenia. Reduced levels of dysbindin mRNA and protein in the hippocampal formation of schizophrenia patients further support involvement of this locus in disease risk. Here, we discuss phylogenetically conserved dysbindin molecular interactions that define its contribution to the assembly of the biogenesis of lysosome-related organelles complex-1 (BLOC-1). We explore fundamental cellular processes where dysbindin and the dysbindin-containing BLOC-1 complex are implicated. We propose that cellular, tissue, and system neurological phenotypes from dysbindin deficiencies in model genetic organisms, and likely individuals affected with schizophrenia, emerge from abnormalities in few core cellular mechanisms controlled by BLOC-1-dysbindin-containing complex rather than from defects in dysbindin itself.
journal_name
Mol Neurobioljournal_title
Molecular neurobiologyauthors
Mullin AP,Gokhale A,Larimore J,Faundez Vdoi
10.1007/s12035-011-8183-3subject
Has Abstractpub_date
2011-08-01 00:00:00pages
53-64issue
1eissn
0893-7648issn
1559-1182journal_volume
44pub_type
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