Fluorescent labeling of SPOCK1 and localization studies in live neural cell lines

Karaboğa, Zeynep Eda
Alzheimer's disease is the most common form of dementia and is incurable. The late onset Alzheimer’s disease (LOAD) is associated with complex genetic transition, and the molecular background has not been enlightened yet. Our previous research on the meta-analysis of genome-wide association studies (GWAS) showed a statistical correlation between SPOCK1 variants and LOAD. Also, it is co-regulated with apolipoprotein (APP), one of the proteins clinically linked with LOAD. Furthermore, the SPOCK1 protein recently had considerable attention due to its role in cell adhesion in various cancers. Considering the current literature on SPOCK1, we hypothesized that SPOCK1 might impact Alzheimer's pathogenesis in neural cells. In this study, human neuroblastoma and astroglia cells expressing fluorescent tagged SPOCK1 were constructed to study the expression and localization of SPOCK1. IHC and confocal image analysis with various organelle labels were performed, and co-localization data showed SPOCK1 localized in mitochondria for both neuroblastoma and astroglial cells. The data obtained in this study related to the localization of SPOCK1 in vitro could contribute to the research of the molecular background of Alzheimer’s disease in the future.


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Alzheimer’s disease is currently the most common cause of dementia in the world. It is a neurodegenerative disease that is diagnosed neuropathologically by observing B-amyloid plaques and neurofibrillary tangles in the brain. Transcriptional differentiations, protein regulations, and the interactions in between have been investigated by recent studies to understand from which brain cell type the disease stems, such as microglia, astrocytes, and neurons. These studies are mostly performed on brain tiss...
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Citation Formats
Z. E. Karaboğa, “Fluorescent labeling of SPOCK1 and localization studies in live neural cell lines,” M.S. - Master of Science, Middle East Technical University, 2022.