• Genomics & Informatics
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• 제8권2호
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• pp.90-93
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• 2010

A-kinase-anchoring proteins (AKAPs) are scaffold proteins which compartmentalize protein kinase A (PKA, cAMP-dependent protein kinase) and other enzymes to specific subcellular sites. The spatiotemporal control of these enzymes by AKAPs is important for cellular function like cell growth and development etc. Hence, it is important to understand the basic function of AKAPs and their functional domains. However, diverse names, function, cellular localizations and many members of AKAPs increase difficulties when researchers search appropriate AKAPs for their experimental purpose. Nevertheless, there was no previous AKAPs-related database regardless of their important cellular functions and difficulty of finding appropriate AKAPs. So, we developed AKAPs database (AKAPDB), which contains their sequence information, functions and other information derived from prediction programs and other databases. Therefore, we propose that AKAPDB can be an important tool to researchers in the related fields. AKAPDB is available via the internet at http://plaza3.snu.ac.kr/akapdb/.

• The Korean Journal of Physiology and Pharmacology
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• 제9권1호
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• pp.9-15
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• 2005

We attempted to analyze the mechanism of polychlorinated biphenyl (PCB)-induced neurotoxicity and identify the target molecules in the neuronal cells for PCBs.Since the developing neuron is particularly sensitive to PCB-induced neurotoxicity, we isolated cerebellar granule cells derived from 7-day old Sprague Dawley (SD) rats and grew cells in culture for additional 7 days to mimic PND-14 conditions. Only non-coplanar PCBs at a high dose showed a significant increase of total protein kinase C (PKC) activity at phobol 12,13-dibutyrate ([$^3M$]PDBu) binding assay, indicating that non-coplanar PCBs are more neuroactive than coplanar PCBs in neuronal cells. PKC isozymes were immunoblotted with the selected monoclonal antibodies. PKC-${\alpha}$, ${\delta}$, and ε were activated with non-coplanar PCB exposure. Receptor for activated C kinase-1 (RACK-1), anchoring protein for activated PKC, was more induced with exposure to coplanar PCBs than non-coplanar PCBs. Reverse transcription PCR (RT-PCR) analysis showed induction of neurogranin (RC-3) and growth associated protein-43 (GAP-43) mRNA with non-coplanar PCBs. The results indicate that these factors may be useful biomarkers for differentiating non-coplanar PCBs from coplanar PCBs. The present study demonstrated that non-coplanar PCBs are more neuroactive congeners than coplanar PCBs.

• BMB Reports
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• 제52권8호
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• pp.526-531
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• 2019

The vertebrate body plan is accomplished by left-right asymmetric organ development and the heart is a representative asymmetric internal organ which jogs to the left-side. Kupffer's vesicle (KV) is a spherical left-right organizer during zebrafish embryogenesis and is derived from a cluster of dorsal forerunner cells (DFCs). Cadherin1 is required for collective migration of a DFC cluster and failure of DFC collective migration by Cadherin1 decrement causes KV malformation which results in defective heart laterality. Recently, loss of function mutation of A-kinase anchoring protein 12 (AKAP12) is reported as a high-risk gene in congenital heart disease patients. In this study, we demonstrated the role of $akap12{\beta}$ in asymmetric heart development. The $akap12{\beta}$, one of the akap12 isoforms, was expressed in DFCs which give rise to KV and $akap12{\beta}$-deficient zebrafish embryos showed defective heart laterality due to the fragmentation of DFC clusters which resulted in KV malformation. DFC-specific loss of $akap12{\beta}$ also led to defective heart laterality as a consequence of the failure of collective migration by cadherin1 reduction. Exogenous $akap12{\beta}$ mRNA not only restored the defective heart laterality but also increased cadherin1 expression in $akap12{\beta}$ morphant zebrafish embryos. Taken together, these findings provide the first experimental evidence that $akap12{\beta}$ regulates heart laterality via cadherin1.