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Yun, Un-Jung,Park, Sang-Eun,Shin, Deug-Y Korean Society for Biochemistry and Molecular Bion 2011 Experimental and molecular medicine Vol.43 No.7
Cellular senescence is a tumor-suppressive process instigated by proliferation in the absence of telomere replication, by cellular stresses such as oncogene activation, or by activation of the tumor suppressor proteins, such as Rb or p53. This process is characterized by an irreversible cell cycle exit, a unique morphology, and expression of senescence-associated-${\beta}$-galactosidase (SA-${\beta}$-gal). Despite the potential biological importance of cellular senescence, little is known of the mechanisms leading to the senescent phenotype. p41-Arc has been known to be a putative regulatory component of the mammalian Arp2/3 complex, which is required for the formation of branched networks of actin filaments at the cell cortex. In this study, we demonstrate that p41-Arc can induce senescent phenotypes when it is overexpressed in human tumor cell line, SaOs-2, which is deficient in p53 and Rb tumor suppressor genes, implying that p41 can induce senescence in a p53-independent way. p41-Arc overexpression causes a change in actin filaments, accumulating actin filaments in nuclei. Therefore, these results imply that a change in actin filament can trigger an intrinsic senescence program in the absence of p53 and Rb tumor suppressor genes.
Novel 2,4-dianilino-5-fluoropyrimidine derivatives possessing ALK inhibitory activities
Yun, Jeong In,Yang, Eun Hye,Latif, Muhammad,Lee, Hyeon Ji,Lee, Kwangho,Yun, Chang-Soo,Park, Chi Hoon,Lee, Chong Ock,Chae, Chong Hak,Cho, Sung Yun,Jung, Hee Jung,Kim, Pilho,Choi, Sang Un,Kim, Hyoung Ra 대한약학회 2014 Archives of Pharmacal Research Vol.37 No.7
A new series of 2,4-dianilino-5-fluoropyrimidine derivatives were designed and synthesized and their anaplastic lymphoma kinase (ALK) inhibitory activities were evaluated by biochemical and cell-based assays in order to discover a new ALK inhibitor. Most compounds synthesized showed good inhibitory activities against ALK and good cytotoxic activities in H3122 cell line. The best compound 6f showed good activity against wild-type ALK along with crizotinib-resistant mutant ALK, and it showed 6 times better activity in cell-based assay than crizotinib. Some SAR studies were performed by the comparisons of the activities between 6 and the designed-synthesized compounds.
Un-jun Hyoung,Yun-jung Yang,Soo-kyoung Kwon,유재형,Soon-chul Myoung,Sae-chul Kim,홍연표 대한예방의학회 2007 예방의학회지 Vol.40 No.2
Objectives : Bisphenol A diglycidyl ether (BADGE) is the major component in commercial liquid epoxy resins, which are manufactured by co-reacting bisphenol A with epichlorohydrin. This study was performed to show the developmental effects of prenatal and postnatal exposures to BADGE in male rat offspring. Methods : Mated female rats were divided into four groups, each containing 12 rats. The dosing solutions were prepared by thoroughly mixing BADGE in corn oil at the 0, 375, 1500 and 3000 mg/kg/day concentrations. Mated females were dosed once daily by oral gavage on gestation day (GD) 6 - 20 and postnatal day (PND) 0 - 21. Pregnant female dams were observed general symptoms and body weight. Also, male pups were observed the general symptoms, body weight, developmental parameters (e.g. anogenital distance, pina detachment, incisor eruption, nipple retention, eye opening, testis descent), organ pathologic changes and hormone levels of plasma. Results : Pregnant rats treated with BADGE died at a rate of about 70% in the 1500 mg/kg/day group and all rats treated with 3000 mg/kg/day died. Body weight, for male pups treated with doses of 375 mg/kg/day, was significantly lower than in the control group at PND 42, 56, and 63 (p<0.05). Evaluation of body characteristics including; separation of auricle, eruption of incisor, separation of eyelid, nipple retention, descent of testis, and separation of the prepuce in the BADGE treated group showed no difference in comparisons with the control group. AGD and adjusted AGD (mm/kg) for general developmental items in BADGE 375 mg/kg/day treated pups tended to be longer than in controls, however, these differences were not statistically significant. Relative weights of adrenal gland, lung (p<0.05), brain, epididymis, prostate, and testis (p<0.01) were heavier than in control in measures at PND 9 weeks. There were no significant changes in comparisons of histological findings of these organs. Loss of spermatids was observed in the seminiferous tubule at PND 9 weeks, but no weight changes were observed. The plasma estrogen levels were similar in the control and treatment groups at PND 3, 6 and 9 weeks. The plasma testosterone levels in the control group tended to increase with age. However, in the BADGE 375 mg/kg/day treated male pups it did not tend to increase. Conclusions : These findings suggest that BADGE is a chemical that has developmental effects consistent with it being an endocrine disruptor.
Un-Jung Yun,박희동,신득용 대한암학회 2006 Cancer Research and Treatment Vol.38 No.4
Recent studies have suggested that p53 regulates the G2 checkpoint in the cell cycle and this function is required for the maintenance of genomic integrity. In this study, we addressed a role of p53 in escaping from cell cycle G2 arrest following DNA damage.Materials and Methods: Cell cycle checkpoint arrest in the human colon cancer cell line HCT116 and its derivatives carry p53 or p21 deletions, were examined by FACS analysis, immunoprecipitation, Western blot and IP-kinase assay.Results: While the cells with functional p53 were arrested at both the G1 and G2 checkpoints, the p53-deficient cells failed to arrest at G1, but they were arrested at G2. However, the p53-deficient cells failed to sustain G2 checkpoint arrest and they entered mitosis earlier than did the p53-positive cells and so this resulted in extensive cell death. Cdc2 kinase becomes reactivated in p53-deficient cells in association with entry into mitosis, but not in the p53-positive cells. Upon DNA damage, the p21-deficient cells, like the p53-negative cells, not only failed to repress cdk2- dependent NF-Y phosphorylation, but they also failed to repress the expression of such cell cycle G2-regulatory genes as cdc2, cyclin B, RNR-R2 and cdc25C, which have all been previously reported as targets of NF-Y transcription factor.Conclusion: p53 is essential to prevent immature escaping from cell cycle G2 checkpoint arrest through p21-mediated cdk2 inactivation, and this leads to inhibition of cdk2-dependent NF-Y phosphorylation and NF-Y dependent transcription of the cell cycle G2-rgulatory genes, including cdc2 and cyclin B. (Cancer Res Treat. 2006;38:224-228)
송유림,Jang Mi Hee,Jang Boyun,Bae Su Jin,Bak Seon Been,Lee Sung Min,Yun Un-Jung,Lee Ju Hee,Park Sang Mi,Jung Dae Hwa,Sa Bok Suk,Song Jong Kuk,이은혜,김광연,Park Kwang-Il,김영우,김상찬 대한독성 유전단백체 학회 2022 Molecular & cellular toxicology Vol.18 No.2
Background Herbal prescriptions have various effects and their efficacy is potentiated by the use of combinations of medicinal herbs. Objective Jageum-Jung (JGJ) is a traditional oriental medical prescription composed of five herbs. It has been used for detoxifi cation, and as an anti-inflammatory and antitumor agent. However, the effect of JGJ on hepatic fibrogenesis is unclear. Results We investigated the role of JGJ in TGF-β1/smad signaling, which is implicated in fibrogenesis, and its hepatoprotective effect in CCl 4 -treated mice with liver fi brosis. Treatment of LX-2 cells with TGF-β induced expression of mediators (α-SMA, PAI-1, and MMP-2) of fibrogenesis and activation of proinflammatory cytokines (TNF-α, IL-1β, and IL-6). However, these were downregulated by pretreatment with JGJ. In mice, oral administration of JGJ prevented liver injury induced by CCl 4 , as indicated by decreases in the ALT and AST levels. Conclusions JGJ inhibits hepatic fibrogenesis and TGF-β1/Smad signaling.