کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8259158 | 1534631 | 2016 | 43 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Schizophrenia susceptibility gene product dysbindin-1 regulates the homeostasis of cyclin D1
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کلمات کلیدی
Cyclin D1nESDMEMFBSMBPDPCGFPCDKPAGEBLOC-1Dulbecco's modified Eagle's medium - Medal of Eagle اصلاح شده DulbeccoSchizophrenia - اسکیزوفرنی یا شیزوفرنیpolyacrylamide gel electrophoresis - الکتروفورز ژل پلی آکریل آمیدImmunoprecipitation - تخریب ایمنیDysbindin-1 - دیزبیندین-1fetal bovine serum - سرم جنین گاوnuclear export signal - سیگنال صادرات هسته ایdystrophin-associated glycoprotein complex - مجموعه گلیکوپروتئین مرتبط با دیستروفینgreen fluorescent protein - پروتئین فلورسنت سبزmaltose binding protein - پروتئین متصل به مالتوزcyclin-dependent kinase - کییناز وابسته به سیکلین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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چکیده انگلیسی
Dysbindin-1 (dystrobrevin binding protein-1, DTNBP1) is now widely accepted as a potential schizophrenia susceptibility gene and accumulating evidence indicates its functions in the neural development. In this study, we tried to identify new binding partners for dysbindin-1 to clarify the novel function of this molecule. When consulted with BioGRID protein interaction database, cyclin D3 was found to be a possible binding partner for dysbindin-1. We then examined the interaction between various dysbindin-1 isoforms (dysbindin-1A, -1B and -1C) and all three D-type cyclins (cyclin D1, D2, and D3) by immunoprecipitation with the COS7 cell expression system, and found that dysbindin-1A preferentially interacts with cyclin D1. The mode of interaction between these molecules was considered as direct binding since recombinant dysbindin-1A and cyclin D1 formed a complex in vitro. Mapping analyses revealed that the C-terminal region of dysbindin-1A binds to the C-terminal of cyclin D1. Consistent with the results of the biochemical analyses, endogenous dysbindin-1was partially colocalized with cyclin D1 in NIH3T3 fibroblast cells and in neuronal stem and/or progenitor cells in embryonic mouse brain. While co-expression of dysbindin-1A with cyclin D1 changed the localization of the latter from the nucleus to cytosol, cyclin D1-binding partner CDK4 inhibited the dysbindin-cyclin D1 interaction. Meanwhile, depletion of endogenous dysbindin-1A increased cyclin D1 expression. These results indicate that dysbindin-1A may control the cyclin D1 function spatiotemporally and might contribute to better understanding of the pathophysiology of dysbindin-1-associated disorders.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1862, Issue 8, August 2016, Pages 1383-1391
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1862, Issue 8, August 2016, Pages 1383-1391
نویسندگان
Hidenori Ito, Rika Morishita, Koh-ichi Nagata,