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Anion Receptors Selective for Oxoanions of Phosphorus and the Importance of Partial Charge
손대협,온탁범,Eunbi Han,Amol Balu Atar,Seung Joo Cho,JONGMINKANG 대한화학회 2021 Bulletin of the Korean Chemical Society Vol.42 No.2
We have developed new symmetric receptors 1 and 2, which bind selectively to oxoanions of phosphorus such as phosphinates and dihydrogen phosphate. Among the phosphinates and dihydrogen phosphate, we have investigated the orders of binding affinities to receptors 1 and 2 are Me2PO2??>?H2PO4??>?PhHPO2? and Me2PO2??>?H2PO4?, respectively. We further investigated the physicochemical reasons for this order by theoretical calculations. Calculation results were in good agreement with experimental results. The order of affinity for the anions seemed to depend on the magnitude of the partial charge of oxygen (hydrogen bond acceptor) present in the anion.
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The Role of Stress Granules in the Neuronal Differentiation of Stem Cells
정신구,온탁범,Chul Ho Jang,Karthikeyan Vijayakumar,조광원 한국분자세포생물학회 2020 Molecules and cells Vol.43 No.10
Cells assemble stress granules (SGs) to protect their RNAs from exposure to harmful chemical reactions induced by environmental stress. These SGs release RNAs, which resume translation once the stress is relieved. During stem cell differentiation, gene expression is altered to allow cells to adopt various functional and morphological features necessary to differentiate. This process induces stress within a cell, and cells that cannot overcome this stress die. Here, we investigated the role of SGs in the progression of stem cell differentiation. SGs aggregated during the neuronal differentiation of human bone marrow-mesenchymal stem cells, and not in cell lines that could not undergo differentiation. SGs were observed between one and three hours post-induction; RNA translation was restrained at the same time. Immediately after disassembly of SGs, the expression of the neuronal marker neurofilament-M (NFM) gradually increased. Assembled SGs that persisted in cells were exposed to salubrinal, which inhibited the dephosphorylation of eukaryotic translation initiation factor 2 subunit 1 (eIF2α), and in eIF2α/S51D mutant cells. When eIF2α/S51A mutant cells differentiated, SGs were not assembled. In all experiments, the disruption of SGs was accompanied by delayed NF-M expression and the number of neuronally differentiated cells was decreased. Decreased differentiation was accompanied by decreased cell viability, indicating the necessity of SGs for preventing cell death during neuronal differentiation. Collectively, these results demonstrate the essential role of SGs during the neuronal differentiation of stem cells.
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김지호,장인엽,Wooje Lee,온탁범 조선대학교 기초과학연구원 2019 조선자연과학논문집 Vol.12 No.4
Programmed cell death 4 (PDCD4) is a novel tumor suppressor that function in the nucleus and the cytoplasm and appears to be involved in the regulation of transcription and translation. Stress granules (SGs) are cytoplasmic foci at which untranslated mRNAs accumulate when cells exposed to environmental stresses. Since PDCD4 has implicated in translation repression through direct interaction with eukaryotic translation initiation factor 4A (eIF4A), we here investigated if PDCD4 has a functional role in the process of SG assembly under oxidative stresses. Using immunofluorescence microscopy, we found that PDCD4 is localized to SGs under oxidative stresses. Next, we tested if knockdown of PDCD4 has an effect on the assembly of SG using PDCD4-specific siRNA. Interestingly, SG assembly was accelerated and this effect was caused by sensitization of phosphorylation of eIF2 and dephosphorylation of eIF4E binding protein (4E-BP). These results suggest that PDCD4 has an effect on SG dynamics and possibly involved in capdependent translation repression under stress conditions.
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Loss of MeCP2 causes subtle alteration in dendritic arborization of retinal ganglion cells
이우제,라메쉬 마리압판,Koushitak De,온탁범 한국통합생물학회 2021 Animal cells and systems Vol.25 No.2
Methyl-CpG-binding protein (MeCP2) is highly expressed in neurons. It plays an important role in the development of synapses and the formation of circuits in the central nervous system (CNS). Mutations in MECP2 cause neurodevelopmental disorders and mental retardation in humans. Therefore, it has become important to determine the distribution and function of MeCP2 in vivo. The retina consists of three nuclear cell layers and two layers of synapses; neurons in each layer are connected to form fine circuits necessary for visual signal transduction. Using immunohistochemical analysis, we found that MeCP2 was expressed in all nuclear cell layers, with differences in the levels of MeCP2 expression observed among the layers. To understand the structural defects in the retina due to the loss of MeCP2, we sought to elucidate the organization of the retinal structure in the Mecp2 knockout (KO) mouse. Overall, we found a normal retinal structure in Mecp2 KO mice. However, because Mecp2 mutations have a highly variable effect on neuronal architecture, we analyzed morphological changes in a subset of retinal ganglion cells of Mecp2 KO mice. In Thy1-GFP mice crossed with Mecp2 mutant mice, Sholl intersections analyses showed a subtle increase in number of intersections due to increased branching proximal to the soma in Mecp2 KO mice. Our results demonstrate that the expression of MeCP2 and the effects of Mecp2 mutations are highly specific to tissue and cell types.
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miR-27 regulates mitochondrial networks by directly targeting the mitochondrial fission factor
탁효선,이은경,김지혜,남석우,이희진,Aravinth kumar Jayabalan,강호인,조동형,온탁범,김욱 생화학분자생물학회 2014 Experimental and molecular medicine Vol.46 No.-
Mitochondrial morphology is dynamically regulated by forming small, fragmented units or interconnected networks, and this is a pivotal process that is used to maintain mitochondrial homeostasis. Although dysregulation of mitochondrial dynamics is related to the pathogenesis of several human diseases, its molecular mechanism is not fully elucidated. In this study, we demonstrate the potential role of miR-27 in the regulation of mitochondrial dynamics. Mitochondrial fission factor (MFF) mRNA is a direct target of miR-27, whose ectopic expression decreases MFF expression through binding to its 3′-untranslated region. Expression of miR-27 results in the elongation of mitochondria as well as an increased mitochondrial membrane potential and mitochondrial ATP level. Our results suggest that miR-27 is a novel regulator affecting morphological mitochondrial changes by targeting MFF.
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