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Jang, Byungki,Kim, Ho Won,Kim, Jong-Seok,Kim, Woo Sik,Lee, Bo Ryeong,Kim, Sojeong,Kim, Hongmin,Han, Seung Jung,Ha, Sang-Jun,Shin, Sung Jae Federation of American Societies for Experimental 2015 Journal of Leukocyte Biology Vol.97 No.2
<P>Cl-amidine, which is a small-molecule inhibitor of PAD, has therapeutic potential for inflammation-mediated diseases. However, little is known regarding the manner by which PAD inhibition by Cl-amidine regulates inflammatory conditions. Here, we investigated the effects of PAD inhibition by Cl-amidine on the functioning of DCs, which are pivotal immune cells that mediate inflammatory diseases. When DC maturation was induced by TLR agonists, reduced cytokine levels (IL-6, IL-1 beta, and IL-12p70) were observed in Cl-amidine-treated DCs. Cl-amidine-treated, LPS-activated DCs exhibited alterations in their mature and functional statuses with up-regulated antigen uptake, down-regulated CD80, and MHC molecules. In addition, Cl-amidine-treated DCs dysregulated peptide-MHC class formations. Interestingly, the decreased cytokines were independent of MAPK/NF-kappa B signaling pathways and transcription levels, indicating that PAD inhibition by Cl-amidine may be involved in post-transcriptional steps of cytokine production. Transmission electron microscopy revealed morphotypical changes with reduced dendrites in the Cl-amidine-treated DCs, along with altered cellular compartments, including fragmented ERs and the formation of foamy vesicles. Furthermore, in vitro and in vivo Cl-amidine treatments impaired the proliferation of naive CD4(+) and CD8(+) T cells. Overall, our findings suggest that Cl-amidine has therapeutic potential for treating inflammation-mediated diseases.</P>
Calsenilin, a Presenilin Interactor, Regulates RhoA Signaling and Neurite Outgrowth
Kim, Hee-Jun,Lee, Won-Haeng,Kim, Mo-Jong,Shin, Sunmee,Jang, Byungki,Park, Jae-Bong,Wasco, Wilma,Buxbaum, Joseph D.,Kim, Yong-Sun,Choi, Eun-Kyoung MDPI 2018 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.19 No.4
<P>Calsenilin modulates A-type potassium channels, regulates presenilin-mediated γ-secretase activity, and represses prodynorphin and <I>c-fos</I> genes expression. RhoA is involved in various cellular functions including proliferation, differentiation, migration, transcription, and regulation of the actin cytoskeleton. Although recent studies demonstrate that calsenilin can directly interact with RhoA and that RhoA inactivation is essential for neuritogenesis, it is uncertain whether there is a link between calsenilin and RhoA-regulated neuritogenesis. Here, we investigated the role of calsenilin in RhoA-regulated neuritogenesis using in vitro and in vivo systems. We found that calsenilin induced RhoA inactivation, which accompanied RhoA phosphorylation and the reduced phosphorylation levels of LIM kinase (LIMK) and cofilin. Interestingly, PC12 cells overexpressing either full-length (FL) or the caspase 3-derived C-terminal fragment (CTF) of calsenilin significantly inactivated RhoA through its interaction with RhoA and p190 Rho GTPase-activating protein (p190RhoGAP). In addition, cells expressing FL and the CTF of calsenilin had increased neurite outgrowth compared to cells expressing the N-terminal fragment (NTF) of calsenilin or vector alone. Moreover, Tat-C3 and Y27632 treatment significantly increased the percentage of neurite-bearing cells, neurite length, and the number of neurites in cells. Finally, calsenilin deficiency in the brains of calsenilin-knockout mice significantly interfered with RhoA inactivation. These findings suggest that calsenilin contributes to neuritogenesis through RhoA inactivation.</P>
Sujung Kim,Hualin Nie,Byungki Jun,Jiseong Kim,Jeongeun Lee,Seungill Kim,Ekyune Kim,Sunhyung Kim 한국유전학회 2020 Genes & Genomics Vol.42 No.5
Background Sweet potato is easily propagated by cuttings. But the molecular biological mechanism of adventitious root formation are not yet clear. Objective To understand the molecular mechanisms of adventitious root formation from stem cuttings in sweet potato. Methods RNA-seq analysis was performed using un-rooted stem (0 day) and rooted stem (3 days). Gene Ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, comparison with Arabidopsis transcription factors (TFs) of DEGs were conducted to investigate the characteristics of genes and TFs involved in root formation. In addition, qRT-PCR analysis using roots at 0, 3, 6, 9, and 12 days after planting was performed to confirm RNA-seq reliability and related genes expression. Results 42,459 representative transcripts and 2092 DEGs were obtained through the RNA-seq analysis. The DEGs indicated the GO terms related to the single-organism metabolic process and cell periphery, and involved in the biosynthesis of secondary metabolites, and phenylpropanoid biosynthesis in KEGG pathways. The comparison with Arabidopsis thaliana TF database showed that 3 TFs (WRKY, NAC, bHLH) involved in root formation of sweet potato. qRT-PCR analysis, which was conducted to confirm the reliability of RNA-seq analysis, indicated that some metabolisms including oxidative stress and wounding, transport, hormone may be involved in adventitious root formation. Conclusions The detected genes related to secondary metabolism, some hormone (auxin, gibberellin), transports, etc. and 3 TFs (WRKY, NAC, bHLH) may have functions in adventitious roots formation. This results provide valuable resources for future research on the adventitious root formation of sweet potato.