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O‐GlcNAcase is essential for embryonic development and maintenance of genomic stability
Yang, Yong Ryoul,Song, Minseok,Lee, Ho,Jeon, Yoon,Choi, Eun‐,Jeong,Jang, Hyun‐,Jun,Moon, Hyo Youl,Byun, Ha‐,Young,Kim, Eung‐,Kyun,Kim, Dae Hyun,Lee, Mi Nam,Koh, Ara,Ghim, Jaewa Blackwell Publishing Ltd 2012 Aging cell Vol.11 No.3
<P><B>Summary</B></P><P>Dysregulation of O‐GlcNAc modification catalyzed by O‐GlcNAc transferase (OGT) and O‐GlcNAcase (OGA) contributes to the etiology of chronic diseases of aging, including cancer, cardiovascular disease, type 2 diabetes, and Alzheimer’s disease. Here we found that natural aging in wild‐type mice was marked by a decrease in OGA and OGT protein levels and an increase in O‐GlcNAcylation in various tissues. Genetic disruption of OGA resulted in constitutively elevated O‐GlcNAcylation in embryos and led to neonatal lethality with developmental delay. Importantly, we observed that serum‐stimulated cell cycle entry induced increased O‐GlcNAcylation and decreased its level after release from G2/M arrest, indicating that O‐GlcNAc cycling by OGT and OGA is required for precise cell cycle control. Constitutively, elevated O‐GlcNAcylation by OGA disruption impaired cell proliferation and resulted in mitotic defects with downregulation of mitotic regulators. OGA loss led to mitotic defects including cytokinesis failure and binucleation, increased lagging chromosomes, and micronuclei formation. These findings suggest an important role for O‐GlcNAc cycling by OGA in embryonic development and the regulation of the maintenance of genomic stability linked to the aging process.</P>
A Literature Review of Clinical Studies Using Sa-am Acupuncture
Lim, Jinwoong,Kim, Yong-hwa,Kim, Yu-gon,Jeong, Hyeon-gyo,Shin, Kyung-moon,Shin, Dong-hoon,Jeong, Hwe-joon,Kang, Deok,Yang, Jae-woo,Oh, Ji-hoon,Yoon, Hong-ryoul,Jo, Jae-sung Korean AcupunctureMoxibustion Medicine Society 2021 대한침구의학회지 Vol.38 No.3
Sa-am acupuncture originated in the Chosun Dynasty and is a distinct feature of Korean medicine. It has been used to treat various diseases and conditions in clinical practice however, there is insufficient scientific evidence to support the use of Sa-am acupuncture. We aimed to comprehensively review the clinical studies of Sa-am acupuncture retrieved from national and international databases (MEDLINE, EMBASE, the China National Knowledge Infrastructure, and 3 Korean databases). There were 52 articles reviewed including 29 case studies, 19 randomized controlled trials (RCTs), and 4 uncontrolled trials. Neurological disorders were the most frequently studied, and kidney tonification, and directional supplementation and draining were the most frequently used methods. Overall, the outcomes were generally positive however, there were many additional treatments together with Sa-am acupuncture reported in the case reports, and the quality of evidence was low in the RCTs. Future studies should report the detailed method of practicing Sa-am acupuncture treatment and focus on the specific effect of Sa-am acupuncture with rigorous design to scientifically support the clinical use of Sa-am acupuncture.
Inositide-dependent signaling pathways as new therapeutic targets in myelodysplastic syndromes
Mongiorgi, Sara,Finelli, Carlo,Yang, Yong Ryoul,Clissa, Cristina,McCubrey, James A.,Billi, Anna Maria,Manzoli, Lucia,Suh, Pann-Ghill,Cocco, Lucio,Follo, Matilde Y. Informa UK (Ashley Publications) 2016 Expert opinion on therapeutic targets Vol.20 No.6
Choi, Jang Hyun,Yang, Yong Ryoul,Lee, Seul Ki,Kim, Sun-Hee,Kim, Yun-Hee,Cha, Joo-Young,Oh, Se-Woong,Ha, Jong-Ryul,Ryu, Sung Ho,Suh, Pann-Ghill Wiley (New York Academy of Sciences) 2008 Annals of the New York Academy of Sciences Vol.1138 No.1
<P>3'-Phosphoinositide-dependent kinase-1 (PDK1) has been identified for its ability to phosphorylate and activate Akt. Accumulated studies have shown that the activation of the PDK1/Akt pathway plays a pivotal role in cell survival, proliferation, and tumorigenesis. Therefore, the PDK1/Akt pathway is believed to be a critical target for cancer intervention. In this paper, we report the discovery of a new function of phenothiazines, widely known as antipsychotics, inhibiting PDK1/Akt pathway. Upon epidermal growth factor (EGF) stimulation, phenothiazines specifically suppressed the kinase activity of PDK1 and the phosphorylation level of Akt. The inhibition of PDK1/Akt kinase resulted in suppression of EGF-induced cell growth and induction of apoptosis in human ovary cancer cells. In particular, phenothiazines were highly selective for downstream targets of PDK1/Akt and did not inhibit the activation of phosphatidylinositol 3-kinase (PI3K), EGFR, or extracellular signal-regulated kinase 1/2 (ERK1/2). In particular, phenothiazines effectively suppressed tumor growth in nude mice of human cancer cells. Taken together, these findings provide strong evidence for novel function of phenothiazines, pharmacologically targeting PDK1/Akt for anticancer drug discovery.</P>
김성국,장종수,김호,Yong-Ryoul Yang,서판길 생화학분자생물학회 2011 Experimental and molecular medicine Vol.43 No.3
Phosphatidylinositol phosphates (PtdInsPs) are ubiquitous membrane phospholipids that play diverse roles in cell growth and differentiation. To clarify the regulation mechanism acting on neurofilament light chain (NF-L) self assembly, we examined the effects of various PtdInsPs on this process. We found that PtdInsPs, including PI(4,5)P2, directly bind to the positively charged Arg54 of murine NF-L, and this binding promotes NF-L self assembly in vitro. Mutant NF-L (R53A/R54A) proteins lacking binding affinity to PtdInsPs did not have the same effect, but the mutant NF-L proteins showed greater self assembly than the wild-type in the absence of any PtdInsP. These results collectively suggest that Arg54 plays a pivotal role in NF-L self assembly by binding with PtdInsPs.
Yoo, Hee-Bong,Oh, Donggeun,Song, Jae Yong,Kawaharasaki, Mamoru,Hwang, Jeeseong,Yang, In Chul,Park, Sang-Ryoul Springer-Verlag 2014 METROLOGIA -BERLIN- Vol.51 No.5
<P>This work demonstrates accurate measurement of the amount of substance concentration of low concentration plasmid DNA by counting individual DNA molecules using a high-sensitivity flow cytometric setup. Plasmid DNA is a widely used form of DNA, and its quantity often needs to be accurately determined. This work establishes a reference analytical method for direct quantification of low concentration plasmid DNA prepared as reference standards for polymerase chain reaction-based DNA quantification. The model plasmid DNA pBR322 (4361?bp) was stained with a fluorescent dye and was detected in a flow stream in a micro-fluidic channel with laser-induced fluorescence detection, for which the DNA flow was electro-hydrodynamically focused at the centre of the channel. 200 to 8000 DNA molecules in a ∼1??L sample volume were counted within 2?min in an ‘exhaustive counting’ manner, which facilitated quantitation without calibration. The sample volume was measured and validated from the close agreement of the results of two independent measurement methods, gravimetric determination of water filling the capillary and graphical estimation of actual cross sectional area of the capillary tubing with the image of calibrated scanning electron microscopy. Within the given concentration range, an excellent measurement linearity (<I>R</I><SUP>2</SUP>?=?0.999) was achieved with appropriate data processing for the correction of the events of double molecules (detection of double molecules opposed to single molecule detection assumed, which occurs due to their coincidental passing of the detection zone). The validity of the proposed method was confirmed from the close agreement with the results of quantitation of enzymatically released nucleotides using capillary electrophoresis.</P>
Kim, Sung-Kuk,Kim, Ho,Yang, Yong-Ryoul,Suh, Pann-Ghill,Chang, Jong-Soo Korean Society for Biochemistry and Molecular Bion 2011 Experimental and molecular medicine Vol.43 No.3
Phosphatidylinositol phosphates (PtdInsPs) are ubiquitous membrane phospholipids that play diverse roles in cell growth and differentiation. To clarify the regulation mechanism acting on neurofilament light chain (NF-L) self assembly, we examined the effects of various PtdInsPs on this process. We found that PtdInsPs, including $PI(4,5)P_2$, directly bind to the positively charged $Arg^{54}$ of murine NF-L, and this binding promotes NF-L self assembly $in$ $vitro$. Mutant NF-L (R53A/R54A) proteins lacking binding affinity to PtdInsPs did not have the same effect, but the mutant NF-L proteins showed greater self assembly than the wild-type in the absence of any PtdInsP. These results collectively suggest that $Arg^{54}$ plays a pivotal role in NF-L self assembly by binding with PtdInsPs.
Sang-Hee Chung,Jung Kuk Kim,Yong-Ryoul Yang,Pann-Ghill Suh,장종수,김성국 생화학분자생물학회 2010 Experimental and molecular medicine Vol.42 No.3
Growth factor stimulation induces Y783 phosphorylation of phosphoinositide-specific PLC-γ1, and the subsequent activation of this enzyme in a cellular signaling cascade. Previously, we showed that a double point mutation, Y509A/F510A, of PLC-γ1, abolished interactions with translational elongation factor 1-α. Here, we report that the Y509A/F510A mutant PLC-γ1displayed extremely high levels of Y783 phosphorylation and enhanced catalytic activity, compared to wild-type PLC-γ1, upon treatment of COS7 cells with EGF. In quiescent COS7 cells, the Y509A/F510A mutant PLC-γ1 exhibited a constitutive hydrolytic activity,whereas the wild-type counterpart displayed a basal level of activity. Upon treatment of COS7 cells with EGF, the Y783F mutation in Y509A/F510A PLC-γ1(Y509A/F510A/Y783F triple mutant) cells also led to an enhanced catalytic activity, whereas Y783F mutation alone displayed a basal level of activity. Our results collectively suggest that the Y509A/F510A mutant is more susceptible to receptor tyrosine kinase-induced Y783phosphorylation than is wild-type PLC-γ1, but no longer requires Y783 phosphorylation step for the Y509A/F510A mutant PLC-γ1 activation in vivo.
Koh, Ara,Lee, Mi Nam,Yang, Yong Ryoul,Jeong, Heeyoon,Ghim, Jaewang,Noh, Jeongeun,Kim, Jaeyoon,Ryu, Dongryeol,Park, Sehoon,Song, Parkyong,Koo, Seung-Hoi,Leslie, Nick R.,Berggren, Per-Olof,Choi, Jang Hy American Society for Microbiology 2013 Molecular and cellular biology Vol.33 No.8
<P>Muscle atrophy occurs under various catabolic conditions, including insulin deficiency, insulin resistance, or increased levels of glucocorticoids. This results from reduced levels of insulin receptor substrate 1 (IRS-1), leading to decreased phosphatidylinositol 3-kinase activity and thereby activation of FoxO transcription factors. However, the precise mechanism of reduced IRS-1 under a catabolic condition is unknown. Here, we report that C1-Ten is a novel protein tyrosine phosphatase (PTPase) of IRS-1 that acts as a mediator to reduce IRS-1 under a catabolic condition, resulting in muscle atrophy. C1-Ten preferentially dephosphorylated Y612 of IRS-1, which accelerated IRS-1 degradation. These findings suggest a novel type of IRS-1 degradation mechanism which is dependent on C1-Ten and extends our understanding of the molecular mechanism of muscle atrophy under catabolic conditions. C1-Ten expression is increased by catabolic glucocorticoid and decreased by anabolic insulin. Reflecting these hormonal regulations, the muscle C1-Ten is upregulated in atrophy but downregulated in hypertrophy. This reveals a previously unidentified role of C1-Ten as a relevant PTPase contributing to skeletal muscle atrophy.</P>