A novel role for 14-3-3ζ in coordinating interneuron development through regulation of Rac1 and non-canonical Shh signalling /
Files
(Published version)
Date
2017
Authors
Greenberg, Zarina Isis,
Editors
Advisors
Journal Title
Journal ISSN
Volume Title
Type:
thesis
Citation
Statement of Responsibility
Conference Name
Abstract
Schizophrenia is a devastating neurodevelopmental disorder widely believed to arise from defects during brain development. Indeed, dysfunction in the formation and function of GABAergic cortical interneurons has been implicated as a central pathogenic mechanism in this, and other, neurodevelopmental disorders. 14-3-3ζ is part of a family of highly conserved intracellular proteins, that bind to the phosphoserine/theronine sites on target proteins and is highly expressed in the brain. Interestingly, several findings in recent years implicate 14-3-3ζ as a candidate risk factor for schizophrenia including: 1) 14-3-3ζ is downregulated in post-mortem schizophrenic brain samples at the mRNA level; 2) 14-3-3ζ is downregulated across multiple neuroproteomic studies on schizophrenia patient samples; 3) linkage studies have implicated 14-3-3 family proteins in numerous neurodevelopmental disorders, and 4) genetic mutations in the gene encoding 14-3-3ζ (YWHAZ) have been found in schizophrenia patients. Previous studies have shown that 14-3-3ζ KO mice exhibit anatomical and behavioural traits akin to those seen in schizophrenia and other neurodevelopmental disorders.
School/Discipline
University of South Australia. School of Pharmacy and Medical Sciences.
School of Pharmacy and Medical Sciences.
School of Pharmacy and Medical Sciences.
Dissertation Note
Thesis (PhD(Medical Science))--University of South Australia, 2017.
Provenance
Copyright 2017 Zarina Isis Greenberg.
Description
1 ethesis (xviii, 196 pages) :
illustrations (some colour), charts (some colour)
Includes bibliographical references (pages 159-184)
illustrations (some colour), charts (some colour)
Includes bibliographical references (pages 159-184)
Access Status
506 0#$fstar $2Unrestricted online access