|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | MEF2C regulates osteoclastogenesis and pathologic bone resorption via c-FOS显示文摘Osteoporosis is a metabolic bone disease with dysregulated coupling between bone resorption and bone formation,which results in decreased bone mineral density.The MEF2C locus,which encodes the transcription factor MADS box transcription enhancer factor 2,polypeptide C(MEF2C),is strongly associated with adult osteoporosis and osteoporotic fractures.Although the role of MEF2C in bone and cartilage formation by osteoblasts,osteocytes,and chondrocytes has been studied,the role of MEF2C in osteoclasts,which mediate bone resorption,remains unclear.In this study,we identified MEF2C as a positive regulator of human and mouse osteoclast differentiation.While decreased MEF2C expression resulted in diminished osteoclastogenesis,ectopic expression of MEF2C enhanced osteoclast generation.Using transcriptomic and bioinformatic approaches,we found that MEF2C promotes the RANKL-mediated induction of the transcription factors c-FOS and NFATc1,which play a key role in osteoclastogenesis.Mechanistically,MEF2C binds to FOS regulatory regions to induce c-FOS expression,leading to the activation of NFATC1 and downstream osteoclastogenesis.Inducible deletion of Mef2c in mice resulted in increased bone mass under physiological conditions and protected mice from bone erosion by diminishing osteoclast formation in K/BxN serum induced arthritis,a murine model of inflammatory arthritis.Our findings reveal direct regulation of osteoclasts by MEF2C,thus adding osteoclasts as a cell type in which altered MEF2C expression or function can contribute to pathological bone remodeling. | Takayuki Fujii Koichi Murata Se-Hwan Mun Seyeon Bae Ye Ji Lee Tannia Pannellini Kyuho Kang David Oliver Kyung-Hyun Park-Min Lionel B.Ivashkiv | 2021 | Bone Research2021，9，1： | 4 |
| 2 | Phase-pure Na3V2(PO4)2F3 embedded in carbon matrix through a facile polyol synthesis as a potential cathode for high performance sodium-ion batteries显示文摘In this study,a pseudo-layered Na super-ionic conductor of Na3V2(PO4)2F3 (NVPF)/C cathode for sodium-ion batteries is prepared successfully using a facile polyol refluxing process without any impurity phases.The X-ray diffraction and Rietveld refinement results confirm that NVPF possesses tetragonal NASICON-type lattice with a space group of P42/mnm.In this preparative method,polyol is utilized as a solvent as well as a carbon source.The presence of nanosized NVPF particles in the carbon network is confirmed by field-emission scanning electron microscopy (FE-SEM) and high-resolution transmission electron microscopy (HR-TEM).The existence of carbon is analyzed by Raman scattering and elemental analysis.When applied as a Na-storage material in a potential window of 2.0-4.3 V,the electrode exhibits two flat voltage plateaus at 3.7 and 4.2 V with an electrochemically active V^3+/V^4+ redox couple.In addition,Na3V2(PO4)2F3/C composite achieved a retention capacity of ~ 88% even after 1,500 cycles at 15 C.Moreover,at high current densities of 30 and 50 C,Na3V2(PO4)2F3/C cathode retains the specific discharge capacities of 108.4 and 105.9 mAh·g-1,respectively,revealing the structural stability of the material prepared through a facile polyol refluxing method. | Sohyun Park Jinju Song Seyeon Kim Balaji Sambandam Vinod Mathew Sungjin Kim Jeonggeun Jo Seokhun Kim Jaekook Kim | 2019 | Nano Research2019，12，4： | 4 |
| 3 | Augmenting MNK1/2 activation by c-FMS proteolysis promotes osteoclastogenesis and arthritic bone erosion显示文摘Osteoclasts are bone-resorbing cells that play an essential role in homeostatic bone remodeling and pathological bone erosion.Macrophage colony stimulating factor(M-CSF)is abundant in rheumatoid arthritis(RA).However,the role of M-CSF in arthritic bone erosion is not completely understood.Here,we show that M-CSF can promote osteoclastogenesis by triggering the proteolysis of c-FMS,a receptor for M-CSF,leading to the generation of FMS intracellular domain(FICD)fragments.Increased levels of FICD fragments positively regulated osteoclastogenesis but had no effect on inflammatory responses.Moreover,myeloid cell-specific FICD expression in mice resulted in significantly increased osteoclast-mediated bone resorption in an inflammatory arthritis model.The FICD formed a complex with DAP5,and the FICD/DAP5 axis promoted osteoclast differentiation by activating the MNK1/2/EIF4E pathway and enhancing NFATcl protein expression.Moreover,targeting the MNK1/2 pathway diminished arthritic bone erosion.These results identified a novel role of c-FMS proteolysis in osteoclastogenesis and the pathogenesis of arthritic bone erosion. | Se Hwan Mun Seyeon Bae Steven Zeng Brian Oh Carmen Chai Matthew Jundong Kim Haemin Kim George Kalliolias Chitra Lekha Dahia Younseo Oh Tae-Hwan Kim Jong Dae Ji Kyung-Hyun Park-Min | 2021 | Bone Research2021，9，4： | 2 |
| 4 | Design of HTS Toroidal Magnets for a 5MJ SMES 显示文摘 | Seyeon Lee | 2012 | IEEE Transactions on Applied Su- perconductivity2012，22，57： | 1 |
| 5 | Inhibition of fos-jun-DNA complex formation by dihydroguaiaretic acid and in vitro cytotoxic effects on cancer cells显示文摘 | Seyeon Park Dug-Keun Lee Chul -Hak Yang | 1998 | Cancer Let1998，127，12： | 1 |
| 6 | Characteristics of rotating armature type high temperature superconducting generators with dual field windings for the wind turbine显示文摘 | Sang Ho Park Yungil Kim Seyeon Lee | 2015 | IEEE Transactions on Applied Superconductivity2015，25，3： | 1 |
| 7 | RANKL-responsive epigenetic mechanism reprograms macrophages into bone-resorbing osteoclasts显示文摘Monocyte/macrophage lineage cells are highly plastic and can differentiate into various cells under different environmental stimuli. Bone-resorbing osteoclasts are derived from the monocyte/macrophage lineage in response to receptor activator of NF-κB ligand (RANKL). However, the epigenetic signature contributing to the fate commitment of monocyte/macrophage lineage differentiation into human osteoclasts is largely unknown. In this study, we identified RANKL-responsive human osteoclast-specific superenhancers (SEs) and SE-associated enhancer RNAs (SE-eRNAs) by integrating data obtained from ChIP-seq, ATAC-seq, nuclear RNA-seq and PRO-seq analyses. RANKL induced the formation of 200 SEs, which are large clusters of enhancers, while suppressing 148 SEs in macrophages. RANKL-responsive SEs were strongly correlated with genes in the osteoclastogenic program and were selectively increased in human osteoclasts but marginally presented in osteoblasts, CD4+ T cells, and CD34+ cells. In addition to the major transcription factors identified in osteoclasts, we found that BATF binding motifs were highly enriched in RANKL-responsive SEs. The depletion of BATF1/3 inhibited RANKL-induced osteoclast differentiation. Furthermore, we found increased chromatin accessibility in SE regions, where RNA polymerase II was significantly recruited to induce the extragenic transcription of SE-eRNAs, in human osteoclasts. Knocking down SE-eRNAs in the vicinity of the NFATc1 gene diminished the expression of NFATc1, a major regulator of osteoclasts, and osteoclast differentiation. Inhibiting BET proteins suppressed the formation of some RANKL-responsive SEs and NFATc1-associated SEs, and the expression of SE-eRNA:NFATc1. Moreover, SE-eRNA:NFATc1 was highly expressed in the synovial macrophages of rheumatoid arthritis patients exhibiting high-osteoclastogenic potential. Our genome-wide analysis revealed RANKL-inducible SEs and SE-eRNAs as osteoclast-specific signatures, which may contribute to the development of osteoclast-specific therapeutic interventions. | Seyeon Bae Kibyeong Kim Keunsoo Kang Haemin Kim Minjoon Lee Brian Oh Kaichi Kaneko Sungkook Ma Jae Hoon Choi Hojoong Kwak Eun Young Lee Sung Ho Park Kyung-Hyun Park-Min | 2023 | Cellular & Molecular Immunology2023，20，1： | 1 |
| 8 | The effects of high concentrations of vitamin C on cancer cells 显示文摘 | Park Seyeon | 2013 | Nutrients2013，5，9： | 1 |
| 9 | Inhibition oflGF-1 Sig- naling by Genistein: Modulation of E-Cadherin Expression and Dow- nregulation of β-Catenin Signaling in Hormone Refractory PC-3 Pro- state Cancer Cells 显示文摘 | Joomin Lee Jihyeung Ju Seyeon Park | 2012 | Nutr Cancer2012，64，1： | 1 |
| 10 | The inhibitory mechanism of curcumin and its derivative against β-catenin/Tcf signaling显示文摘 | Chi Hoon Park Eun Ryeong Hahm Seyeon Park Hyun-Kyung Kim Chul Hak Yang | 2005 | FEBS Letters2005，，13： | 1 |
| 11 | Comparative studies on the binding site of anesthetics to GABA a receptors using in silico docking methods显示文摘Although the GABAA receptor(GABAAR)has been proposed as the main action site for sevoflurane,isoflurane,halothane,enflurane,propofol,and benzodiazepines(BZDs),binding of these anesthetics with high-resolution structures of the GABAAR have been rarely examined by comparative docking analyses.Moreover,various combinations of ligands on more GABAARs with various subtypes need to be analyzed to understand the elaborate action mechanism of GABAARs better because some GABAA ligands showed specificity toward the distinct subtypes of the GABAAR.Methods:We performed in silico docking analysis to compare the binding modes of sevoflurane,isoflurane,halothane,enflurane,propofol,and BZDs to the GABAAR based on one of the most recently provided 3D structures.We performed the docking analysis and the affinity-based ranking of the binding sites.Results:Our docking studies revealed that isoflurane,halothane,and enflurane docked in an extracellular domain(ECD)on GABAARs,in contrast to sevoflurane.Conclusion:Our results supported a multi-site mechanism for the allosteric modulation of propofol.Propofol was bound to the pore or favored various subsites in the transmembrane domain(TMD).Our result confirmed that different chemically related BZD ligands interact via distinct binding modes rather than by using a common binding mode,as previously suggested. | SEUNGHYUN AHN JUNG-YEON LEE JIHA SUNG HYUN JOO KIM SEYEON PARK | 2023 | BIOCELL2023，47，7： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员