• Molecules and Cells
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• v.40 no.9
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• pp.621-631
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• 2017

Vaccinia-related kinase 1 (VRK1) and VRK3 are members of the VRK family of serine/threonine kinases and are principally localized in the nucleus. Despite the crucial roles of VRK1/VRK3 in physiology and disease, the molecular and functional interactions of VRK1/VRK3 are poorly understood. Here, we identified over 200 unreported VRK1/VRK3-interacting candidate proteins by affinity purification and LC-MS/MS. The networks of VRK1 and VRK3 interactomes were found to be associated with important biological processes such as the cell cycle, DNA repair, chromatin assembly, and RNA processing. Interactions of interacting proteins with VRK1/VRK3 were confirmed by biochemical assays. We also found that phosphorylations of XRCC5 were regulated by both VRK1/VRK3, and that of CCNB1 was regulated by VRK3. In liver cancer cells and tissues, VRK1/VRK3 were highly upregulated and its depletion affected cell cycle progression in the different phases. VRK3 seemed to affect S phase progression and G2 or M phase entry and exit, whereas VRK1 affects G1/S transition in the liver cancer, which could be explained by different interacting candidate proteins. Thus, this study not only provides a resource for investigating the unidentified functions of VRK1/VRK3, but also an insight into the regulatory roles of VRK1/VRK3 in biological processes.

• BMB Reports
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• v.55 no.5
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• pp.244-249
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• 2022

Characterized by abnormal proliferation and migration of vascular smooth muscle cells (VSMCs), neointima hyperplasia is a hallmark of vascular restenosis after percutaneous vascular interventions. Vaccinia-related kinase 1 (VRK1) is a stress adaption-associated ser/thr protein kinase that can induce the proliferation of various types of cells. However, the role of VRK1 in the proliferation and migration of VSMCs and neointima hyperplasia after vascular injury remains unknown. We observed increased expression of VRK1 in VSMCs subjected to platelet-derived growth factor (PDGF)-BB by western blotting. Silencing VRK1 by shVrk1 reduced the number of Ki-67-positive VSMCs and attenuated the migration of VSMCs. Mechanistically, we found that relative expression levels of β-catenin and effectors of mTOR complex 1 (mTORC1) such as phospho (p)-mammalian target of rapamycin (mTOR), p-S6, and p-4EBP1 were decreased after silencing VRK1. Restoration of β-catenin expression by SKL2001 and re-activation of mTORC1 by Tuberous sclerosis 1 siRNA (siTsc1) both abolished shVrk1-mediated inhibitory effect on VSMC proliferation and migration. siTsc1 also rescued the reduced expression of β-catenin caused by VRK1 inhibition. Furthermore, mTORC1 re-activation failed to recover the attenuated proliferation and migration of VSMC resulting from shVrk1 after silencing β-catenin. We also found that the vascular expression of VRK1 was increased after injury. VRK1 inactivation in vivo inhibited vascular injury-induced neointima hyperplasia in a β-catenin-dependent manner. These results demonstrate that inhibition of VRK1 can suppress the proliferation and migration of VSMC and neointima hyperplasia after vascular injury via mTORC1/β-catenin pathway.

• The Korean Journal of Ceramics
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• v.4 no.4
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• pp.286-291
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• 1998

Dielectric properties of $Pb(Mg_{1/3}Nb_{2/3})O_{3}-PbTiO_{3}$, ceramics prepared by the columbite precursor method have been investigated as a function of the sintering temperature in the range of 1000∼$1250^{\circ}C$. The $Pb(Mg_{1/3}Nb_{2/3})O_{3}-PbTiO_{3}$ ceramics show typical relaxor ferroelectric behavior. As the sintering temperature increased, the dielectric constant increased and the phase transition temperature shifted to lower temperature. The TCK(temperature coefficient of dielectric constant) and VRK (variation rate of dielectric constant) increased with increasing sintering temperature. The $Pb(Mg_{1/3}Nb_{2/3})O_{3}-PbTiO_{3}$ compositions sintered at $1250^{\circ}C$ appear to be suitable for ferroelectric bolometer.

• Journal of Animal Science and Technology
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• v.56 no.7
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• pp.23.1-23.7
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• 2014

Background: Scanning of the genome for selection signatures between breeds may play important role in understanding the underlie causes for observable phenotypic variations. The discovery of high density single nucleotide polymorphisms (SNPs) provide a useful starting point to perform genome-wide scan in pig populations in order to identify loci/candidate genes underlie phenotypic variation in pig breeds and facilitate genetic improvement programs. However, prior to this study genomic region under selection in commercially selected Berkshire and Korean native pig breeds has never been detected using high density SNP markers. To this end, we have genotyped 45 animals using Porcine SNP60 chip to detect selection signatures in the genome of the two breeds by using the $F_{ST}$ approach. Results: In the comparison of Berkshire and KNP breeds using the FDIST approach, a total of 1108 outlier loci (3.48%) were significantly different from zero at 99% confidence level with 870 of the outlier SNPs displaying high level of genetic differentiation ($F_{ST}{\geq}0.490$). The identified candidate genes were involved in a wide array of biological processes and molecular functions. Results revealed that 19 candidate genes were enriched in phosphate metabolism (GO: 0006796; ADCK1, ACYP1, CAMK2D, CDK13, CDK13, ERN1, GALK2, INPP1; MAK, MAP2K5, MAP3K1, MAPK14, P14KB, PIK3C3, PRKC1, PTPRK, RNASEL, THBS1, BRAF, VRK1). We have identified a set of candidate genes under selection and have known to be involved in growth, size and pork quality (CART, AGL, CF7L2, MAP2K5, DLK1, GLI3, CA3 and MC3R), ear morphology and size (HMGA2 and SOX5) stress response (ATF2, MSRB3, TMTC3 and SCAF8) and immune response (HCST and RYR1). Conclusions: Some of the genes may be used to facilitate genetic improvement programs. Our results also provide insights for better understanding of the process and influence of breed development on the pattern of genetic variations.