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Effect of Lewis Basic Amine Site on Proton Reduction Activity of NNN-Co Pincer Complex
Song Seungjin,Cho Jaewhan,Jo Hyeonjeong,Lee Junseong,Choi Jun‐Ho,Seo Junhyeok 대한화학회 2021 Bulletin of the Korean Chemical Society Vol.42 No.10
Electrochemical proton reduction is a promising energy storage method because H2 molecule has a simple structure with a relatively low potential energy. Current interest in hydrogen catalysts has increased research efforts on synthetic analogs of hydrogenase active sites. In this study, we demonstrated the electrochemical H2 evolution reactivity of [NNNR -Co(CH3CN)3] 2+ (R CH2 (1b), NCH3 (2b)) complexes and examined a proton-relay process in the H2 evolution reaction (HER). Upon one-electron reduction, the Co(II) ion center in a high-spin state dissociated a CH3CN ligand, while opening a reaction site. Cyclic voltammograms of the Co complexes indicated quasi-reversible Co(II/I) redox behaviors, and both complexes 1b and 2b showed catalytic H2 evolution activity. Interestingly, 2b, assisted by a protonrelaying NCH3 group, exhibited more efficient catalytic activity than 1b.
Kim, Jung-Hoon,Song, Jaewhan,Park, Kye Won Pharmaceutical Society of Korea 2015 Archives of Pharmacal Research Vol.38 No.3
<P>The consumption of high-calorie foods combined with less physical exercise has increased the prevalence of obesity. Obesity is also associated with high blood pressure, atherosclerosis, insulin resistance, diabetes, impaired host defense, and the risk of some cancers. Because PPAR gamma is a central player that participates in various biological responses, including lipid metabolism, inflammation, and cell proliferation, further understanding of the lipid metabolic sensor PPAR gamma is necessary to reduce the incidence of metabolic diseases and cancer.</P>
New role of E3 ubiquitin ligase in the regulation of necroptosis
( Jinho Seo ),( Eun-woo Lee ),( Jaewhan Song ) 생화학분자생물학회 2016 BMB Reports Vol.49 No.5
Necroptosis is a well-known form of caspase-independent cell death. Necroptosis can be triggered by various extrinsic stimuli, including death ligands in the presence of receptorinteracting protein kinase 3 (RIPK3), a key mediator of necroptosis induction. Our recent studies have revealed that C-terminus HSC-70 interacting protein (CHIP), an E3 ligase, can function as an inhibitor of necroptosis. CHIP-/- mouse embryonic fibroblast showed higher sensitivity to necrotic stimuli than wild-type mouse embryonic fibroblast cells. Deleterious effects of CHIP knockout MEFs were retrieved by RIPK3 depletion. We found that CHIP negatively regulated RIPK3 and RIPK1 by ubiquitylation- and lysosome- dependent degradation. In addition, CHIP-/- mice showed postnatal lethality with intestinal defects that could be rescued by crossing with RIPK3-/- mice. These results suggest that CHIP is a negative regulator of RIPK1 and RIPK3, thus inhibiting necroptosis. [BMB Reports 2016; 49(5): 247-248]
Regulatory Network of ARF in Cancer Development
Ko, Aram,Han, Su Yeon,Song, Jaewhan Korean Society for Molecular and Cellular Biology 2018 Molecules and cells Vol.41 No.5
ARF is a tumor suppressor protein that has a pivotal role in the prevention of cancer development through regulating cell proliferation, senescence, and apoptosis. As a factor that induces senescence, the role of ARF as a tumor suppressor is closely linked to the p53-MDM2 axis, which is a key process that restrains tumor formation. Thus, many cancer cells either lack a functional ARF or p53, which enables them to evade cell oncogenic stress-mediated cycle arrest, senescence, or apoptosis. In particular, the ARF gene is a frequent target of genetic and epigenetic alterations including promoter hyper-methylation or gene deletion. However, as many cancer cells still express ARF, pathways that negatively modulate transcriptional or post-translational regulation of ARF could be potentially important means for cancer cells to induce cellular proliferation. These recent findings of regulators affecting ARF protein stability along with its low levels in numerous human cancers indicate the significance of an ARF post-translational mechanism in cancers. Novel findings of regulators stimulating or suppressing ARF function would provide new therapeutic targets to manage cancer- and senescence-related diseases. In this review, we present the current knowledge on the regulation and alterations of ARF expression in human cancers, and indicate the importance of regulators of ARF as a prognostic marker and in potential therapeutic strategies.
Dynamics of ARF regulation that control senescence and cancer
( Aram Ko ),( Su Yeon Han ),( Jaewhan Song ) 생화학분자생물학회 2016 BMB Reports Vol.49 No.11
ARF is an alternative reading frame product of the INK4a/ARF locus, inactivated in numerous human cancers. ARF is a key regulator of cellular senescence, an irreversible cell growth arrest that suppresses tumor cell growth. It functions by sequestering MDM2 (a p53 E3 ligase) in the nucleolus, thus activating p53. Besides MDM2, ARF has numerous other interacting partners that induce either cellular senescence or apoptosis in a p53-independent manner. This further complicates the dynamics of the ARF network. Expression of ARF is frequently disrupted in human cancers, mainly due to epigenetic and transcriptional regulation. Vigorous studies on various transcription factors that either positively or negatively regulate ARF transcription have been carried out. However, recent focus on posttranslational modifications, particularly ubiquitination, indicates wider dynamic controls of ARF than previously known. In this review, we discuss the role and dynamic regulation of ARF in senescence and cancer. [BMB Reports 2016; 49(11): 598-606]