Glucocorticoid receptor alpha and beta isoforms are not mutated in bipolar affective disorder
Autor: | Constantine E. Sekeris, C. Troungos, George Trikkas, Amalia F. Tsolakidou, Paraskevi Moutsatsou |
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Rok vydání: | 2008 |
Předmět: |
Gene isoform
Adult Male medicine.medical_specialty Bipolar Disorder InformationSystems_INFORMATIONSTORAGEANDRETRIEVAL Molecular Sequence Data Biology Peripheral blood mononuclear cell Cellular and Molecular Neuroscience Glucocorticoid receptor Receptors Glucocorticoid Reference Values Internal medicine medicine Genetic predisposition Coding region Humans Protein Isoforms Receptor GeneralLiterature_REFERENCE(e.g. dictionaries encyclopedias glossaries) Molecular Biology Aged Base Sequence Mood Disorders Reverse Transcriptase Polymerase Chain Reaction Middle Aged Ligand (biochemistry) Psychiatry and Mental health Affect Endocrinology ComputingMethodologies_DOCUMENTANDTEXTPROCESSING Female Heteroduplex |
Zdroj: | Molecular Psychiatry 5:2 (Mar2000): 196-202 Molecular Psychiatry 5:2(Mar2000):196-202 |
Popis: | The periodically hyperactive hypothalamic-pituitary-adrenal (HPA) axis in bipolar affective disorders, as well as the reported changes in the binding characteristics of the glucocorticoid receptor (GR), suggest the possible involvement of the GR in the aetiopathology of this disease. This was investigated by screening the coding sequences of both GR isoforms, GRalpha and GRbeta, for the presence of mutations. As a genetic predisposition has been implicated, we included in this study bipolar patients who were siblings. By RT-PCR of peripheral blood mononuclear cells from patients suffering from bipolar illness, using primers spanning the whole length of the GRalpha and GRbeta coding region and subsequent agarose gel electrophoresis, heteroduplex and sequence analyses, no GR mutations could be detected. Since glucocorticoid receptor activity can be modulated by agents other than the respective ligand (eg by growth factors, cytokines and stress signals), our results favor derangements in the modulation of GR activity by such agents and not in the primary structure of the receptor as aetiopathologic factors of bipolar disease. |
Databáze: | OpenAIRE |
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