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  • 1
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    Online Resource
    Effects of exercise‐induced apelin levels on skeletal muscle and their capillarization in type 2 diabetic rats
    Wiley ; 2017
    In:  Muscle & Nerve Vol. 56, No. 6 ( 2017-12), p. 1155-1163
    Details
    In: Muscle & Nerve, Wiley, Vol. 56, No. 6 ( 2017-12), p. 1155-1163
    Abstract: Exercise‐induced apelin as a myokine is believed to play a role in the improvement of type 2 diabetes mellitus (T2DM) and capillarization. In this study, we evaluated the association between exercise‐induced apelin and muscle capillarization. Methods Zucker rats underwent a treadmill exercise program. Body composition, muscle strength, muscle size, muscle capillarization, and insulin resistance (homeostatic model assessment [HOMA‐IR]) were measured. Apelin levels of skeletal muscle and plasma were then analyzed. Results Exercise improved body composition ( P   〈  0.05), HOMA‐IR ( P   〈  0.05), and grip strength ( P   〈  0.001). In the soleus, the fiber size of T2DM was decreased ( P   〈  0.001), but it increased in fiber size and capillarization after exercise ( P   〈  0.001) occurred. We identified an increase in plasma apelin ( P   〈  0.05) and a decrease in soleus apelin ( P   〈  0.01), as well as an association between soleus apelin and angiogenesis ( P   〈  0.01). Discussion A role for exercise‐induced apelin in improving metabolism indicates the possibility of a new drug target for the treatment of metabolic diseases and repairing skeletal muscle damage. Muscle Nerve 56 : 1155–1163, 2017
    Type of Medium: Online Resource
    ISSN: 0148-639X , 1097-4598
    URL: Issue
    URL: Article
    DOI: 10.1002/mus.v56.6
    DOI: 10.1002/mus.25596
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2017
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  • 2
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    Evaluation of treadmill exercise effect on muscular lipid profiles of diabetic fatty rats by nanoflow liquid chromatography–tandem mass spectrometry
    Springer Science and Business Media LLC ; 2016
    In:  Scientific Reports Vol. 6, No. 1 ( 2016-07-08)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 6, No. 1 ( 2016-07-08)
    Abstract: We compare comprehensive quantitative profiling of lipids at the molecular level from skeletal muscle tissues (gastrocnemius and soleus) of Zucker diabetic fatty rats and Zucker lean control rats during treadmill exercise by nanoflow liquid chromatography–tandem mass spectrometry. Because type II diabetes is caused by decreased insulin sensitivity due to excess lipids accumulated in skeletal muscle tissue, lipidomic analysis of muscle tissues under treadmill exercise can help unveil the mechanism of lipid-associated insulin resistance. In total, 314 lipid species, including phospholipids, sphingolipids, ceramides, diacylglycerols (DAGs), and triacylglycerols (TAGs), were analyzed to examine diabetes-related lipid species and responses to treadmill exercise. Most lysophospholipid levels increased with diabetes. While DAG levels (10 from the gastrocnemius and 13 from the soleus) were 〉 3-fold higher in diabetic rats, levels of most of these decreased after exercise in soleus but not in gastrocnemius. Levels of 5 highly abundant TAGs (52:1 and 54:3 in the gastrocnemius and 48:2, 50:2, and 52:4 in the soleus) displaying 2-fold increases in diabetic rats decreased after exercise in the soleus but not in the gastrocnemius in most cases. Thus, aerobic exercise has a stronger influence on lipid levels in the soleus than in the gastrocnemius in type 2 diabetic rats.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/srep29617
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2016
    detail.hit.zdb_id: 2615211-3
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  • 3
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    PIP4K2A as a negative regulator of PI3K in PTEN - deficient glioblastoma
    Rockefeller University Press ; 2019
    In:  Journal of Experimental Medicine Vol. 216, No. 5 ( 2019-05-06), p. 1120-1134
    Details
    In: Journal of Experimental Medicine, Rockefeller University Press, Vol. 216, No. 5 ( 2019-05-06), p. 1120-1134
    Abstract: Glioblastoma (GBM) is the most malignant brain tumor with profound genomic alterations. Tumor suppressor genes regulate multiple signaling networks that restrict cellular proliferation and present barriers to malignant transformation. While bona fide tumor suppressors such as PTEN and TP53 often undergo inactivation due to mutations, there are several genes for which genomic deletion is the primary route for tumor progression. To functionally identify putative tumor suppressors in GBM, we employed in vivo RNAi screening using patient-derived xenograft models. Here, we identified PIP4K2A, whose functional role and clinical relevance remain unexplored in GBM. We discovered that PIP4K2A negatively regulates phosphoinositide 3-kinase (PI3K) signaling via p85/p110 component degradation in PTEN-deficient GBMs and specifically targets p85 for proteasome-mediated degradation. Overexpression of PIP4K2A suppressed cellular and clonogenic growth in vitro and impeded tumor growth in vivo. Our results unravel a novel tumor-suppressive role of PIP4K2A for the first time and support the feasibility of combining oncogenomics with in vivo RNAi screen.
    Type of Medium: Online Resource
    ISSN: 0022-1007 , 1540-9538
    URL: Article
    DOI: 10.1084/jem.20172170
    RVK:
    XA 10000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2019
    detail.hit.zdb_id: 1477240-1
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  • 4
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    Promising Therapeutic Efficacy of GC1118, an Anti-EGFR Antibody, against KRAS Mutation-Driven Colorectal Cancer Patient-Derived Xenografts
    MDPI AG ; 2019
    In:  International Journal of Molecular Sciences Vol. 20, No. 23 ( 2019-11-24), p. 5894-
    Details
    In: International Journal of Molecular Sciences, MDPI AG, Vol. 20, No. 23 ( 2019-11-24), p. 5894-
    Abstract: Epidermal growth factor receptor (EGFR)-targeted monoclonal antibodies, including cetuximab and panitumumab, are used to treat metastatic colorectal cancer (mCRC). However, this treatment is only effective for a small subset of mCRC patients positive for the wild-type KRAS GTPase. GC1118 is a novel, fully humanized anti-EGFR IgG1 antibody that displays potent inhibitory effects on high-affinity EGFR ligand-induced signaling and enhanced antibody-mediated cytotoxicity. In this study, using 51 CRC patient-derived xenografts (PDXs), we showed that KRAS mutants expressed remarkably elevated autocrine levels of high-affinity EGFR ligands compared with wild-type KRAS. In three KRAS-mutant CRCPDXs, GC1118 was more effective than cetuximab, whereas the two agents demonstrated comparable efficacy against three wild-type KRAS PDXs. Persistent phosphatidylinositol-3-kinase (PI3K)/AKT signaling was thought to underlie resistance to GC1118. In support of these findings, a preliminary improved anti-cancer response was observed in a CRC PDX harboring mutated KRAS with intrinsically high AKT activity using GC1118 combined with the dual PI3K/mammalian target of rapamycin (mTOR)/AKT inhibitor BEZ-235, without observed toxicity. Taken together, the superior antitumor efficacy of GC1118 alone or in combination with PI3K/mTOR/AKT inhibitors shows great therapeutic potential for the treatment of KRAS-mutant mCRC with elevated ratios of high- to low-affinity EGFR ligands and PI3K-AKT pathway activation.
    Type of Medium: Online Resource
    ISSN: 1422-0067
    URL: Article
    DOI: 10.3390/ijms20235894
    Language: English
    Publisher: MDPI AG
    Publication Date: 2019
    detail.hit.zdb_id: 2019364-6
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  • 5
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    Scanning accuracy of an intraoral scanner according to different inlay preparation designs
    Springer Science and Business Media LLC ; 2023
    In:  BMC Oral Health Vol. 23, No. 1 ( 2023-07-24)
    Details
    In: BMC Oral Health, Springer Science and Business Media LLC, Vol. 23, No. 1 ( 2023-07-24)
    Abstract: The accuracy of intraoral scanning plays a crucial role in the workflow of computer-assisted design/computer-assisted manufacturing. However, data regarding scanning accuracy for inlay preparation designs are lacking. The purpose of this in vitro study was to evaluate the influence of the depth of the occlusal cavity and width of the gingival floor of the proximal box on the trueness and precision of intraoral scans for inlay restoration. Methods Artificial teeth were used in this study. Four types of preparations for mesio-occlusal inlay were performed on each #36 artificial tooth depending on two different depths of the occlusal cavity (1 mm and 2 mm) and widths of the gingival floor of the proximal box (1.5 mm and 2.5 mm). Artificial teeth were scanned 10 times each with Cerec Primescan AC, and another scan was performed subsequently with a laboratory scanner as a reference ( n  = 10). Standard tessellation language files were analyzed using a three-dimensional analysis software program. Experimental data were analyzed using two-way analysis of variance and the Bonferroni multiple comparison test. Results The narrow shallow group had significantly higher deviation values for trueness than the wide deep group ( p   〈  0.05). The wide deep group had the lowest average deviation value for trueness and there was no significant difference between the narrow deep and wide shallow groups ( p   〉  0.05). For the mean maximum positive deviation, the wide groups had significantly lower values than the narrow groups ( p   〈  0.05). Trueness was affected by both the width and depth( p   〈  0.05), whereas the mean maximum positive deviation was affected by the width ( p   〈  0.05). The mean maximum negative deviation was affected by all three factors ( p   〈  0.05). Precision was affected by the depth and the interaction between the depth of the occlusal cavity and width of the gingival floor ( p   〈  0.05). Conclusions The design of different inlay cavity configurations affected the accuracy of the digital intraoral scanner. The highest average deviation for trueness was observed in the narrow shallow group and the lowest in the wide deep group. With regard to precision, the narrow shallow group showed the lowest average deviation, and the narrow deep group showed highest value.
    Type of Medium: Online Resource
    ISSN: 1472-6831
    URL: Article
    DOI: 10.1186/s12903-023-03233-2
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2091511-1
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  • 6
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    α-Fluoroamine synthesis via P( iii )-mediated deoxygenative geminal fluorosulfonimidation of 1,2-diketones
    Royal Society of Chemistry (RSC) ; 2022
    In:  Organic & Biomolecular Chemistry Vol. 20, No. 16 ( 2022), p. 3263-3267
    Details
    In: Organic & Biomolecular Chemistry, Royal Society of Chemistry (RSC), Vol. 20, No. 16 ( 2022), p. 3263-3267
    Abstract: A deoxygenative geminal fluorosulfonimidation of 1,2-diketones was achieved for the synthesis of tetrasubstituted α-fluoroamines under mild conditions. In this study, a transition metal-free formal N–F insertion of N -fluorobenzenesulfonimide was enabled via the Kukhtin–Ramirez reaction employing a dealkylation-resistant P( iii ) reagent developed in our laboratory. Computational analysis was also performed to obtain a general mechanistic picture, which explained the reactivity and selectivity for this type of reaction.
    Type of Medium: Online Resource
    ISSN: 1477-0520 , 1477-0539
    URL: Article
    DOI: 10.1039/D2OB00498D
    Language: English
    Publisher: Royal Society of Chemistry (RSC)
    Publication Date: 2022
    detail.hit.zdb_id: 2097583-1
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  • 7
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    Ahnak depletion accelerates liver regeneration by modulating the TGF-β/Smad signaling pathway
    Korean Society for Biochemistry and Molecular Biology - BMB Reports ; 2022
    In:  BMB Reports Vol. 55, No. 8 ( 2022-08-31), p. 401-406
    Details
    In: BMB Reports, Korean Society for Biochemistry and Molecular Biology - BMB Reports, Vol. 55, No. 8 ( 2022-08-31), p. 401-406
    Type of Medium: Online Resource
    ISSN: 1976-670X
    URL: Article
    DOI: 10.5483/BMBRep.2022.55.8.071
    Language: English
    Publisher: Korean Society for Biochemistry and Molecular Biology - BMB Reports
    Publication Date: 2022
    detail.hit.zdb_id: 2410393-7
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  • 8
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    O- and N-Methyltransferases in benzylisoquinoline alkaloid producing plants
    Springer Science and Business Media LLC ; 2024
    In:  Genes & Genomics Vol. 46, No. 3 ( 2024-03), p. 367-378
    Details
    In: Genes & Genomics, Springer Science and Business Media LLC, Vol. 46, No. 3 ( 2024-03), p. 367-378
    Type of Medium: Online Resource
    ISSN: 1976-9571 , 2092-9293
    URL: Article
    DOI: 10.1007/s13258-023-01477-4
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2024
    detail.hit.zdb_id: 2504587-8
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  • 9
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    AHNAK Loss in Mice Promotes Type II Pneumocyte Hyperplasia and Lung Tumor Development
    American Association for Cancer Research (AACR) ; 2018
    In:  Molecular Cancer Research Vol. 16, No. 8 ( 2018-08-01), p. 1287-1298
    Details
    In: Molecular Cancer Research, American Association for Cancer Research (AACR), Vol. 16, No. 8 ( 2018-08-01), p. 1287-1298
    Abstract: AHNAK is known to be a tumor suppressor in breast cancer due to its ability to activate the TGFβ signaling pathway. However, the role of AHNAK in lung tumor development and progression remains unknown. Here, the Ahnak gene was disrupted to determine its effect on lung tumorigenesis and the mechanism by which it triggers lung tumor development was investigated. First, AHNAK protein expression was determined to be decreased in human lung adenocarcinomas compared with matched nonneoplastic lung tissues. Then, Ahnak−/− mice were used to investigate the role of AHNAK in pulmonary tumorigenesis. Ahnak−/− mice showed increased lung volume and thicker alveolar walls with type II pneumocyte hyperplasia. Most importantly, approximately 20% of aged Ahnak−/− mice developed lung tumors, and Ahnak−/− mice were more susceptible to urethane-induced pulmonary carcinogenesis than wild-type mice. Mechanistically, Ahnak deficiency promotes the cell growth of lung epithelial cells by suppressing the TGFβ signaling pathway. In addition, increased numbers of M2-like alveolar macrophages (AM) were observed in Ahnak−/− lungs, and the depletion of AMs in Ahnak−/− lungs alleviated lung hyperplastic lesions, suggesting that M2-like AMs promoted the progression of lung hyperplastic lesions in Ahnak-null mice. Collectively, AHNAK suppresses type II pneumocyte proliferation and inhibits tumor-promoting M2 alternative activation of macrophages in mouse lung tissue. These results suggest that AHNAK functions as a novel tumor suppressor in lung cancer. Implications: The tumor suppressor function of AHNAK, in murine lungs, occurs by suppressing alveolar epithelial cell proliferation and modulating lung microenvironment. Mol Cancer Res; 16(8); 1287–98. ©2018 AACR.
    Type of Medium: Online Resource
    ISSN: 1541-7786 , 1557-3125
    URL: Article
    DOI: 10.1158/1541-7786.MCR-17-0726
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
    detail.hit.zdb_id: 2097884-4
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  • 10
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    Abstract 3323: Discovery of a small-molecule inhibitor that can target EGFR with C797S mutation
    American Association for Cancer Research (AACR) ; 2022
    In:  Cancer Research Vol. 82, No. 12_Supplement ( 2022-06-15), p. 3323-3323
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 82, No. 12_Supplement ( 2022-06-15), p. 3323-3323
    Abstract: EGFR is a transmembrane protein that functions as a receptor tyrosine kinase (RTK). Upon ligand binding or by activating mutations (Exon19 deletion, L858R mutation, and others), EGFR turns on the downstream signals that include oncogenic RAS/MEK/ERK, PI3K/AKT/mTOR, and JAK/STAT pathways. EGFR gene mutations and amplifications are frequently found in various human cancers and, in non-small cell lung cancer (NSCLC), the EGFR gene is mutated with 10-15% frequency (about 50% in Asian patients). While the 1st and 2nd generation EGFR inhibitors are effective in targeting EGFR mutants with Exon19 deletion and L858R mutation, additional T790M mutation in the EGFR gene causes resistance. The 3rd generation EGFR inhibitor (Osimertinib) works against EGFR mutants with T790M mutation; however, another EGFR mutation occurs at the amino acid 797 position (C797S), which makes Osimertinib ineffective. This is one of the major resistance mechanisms in Osimertinib-treated patients, and the 4th generation EGFR inhibitor that can target the C797S mutant is needed. We developed a compound that effectively disables various EGFR mutations, including Del19/T790M/C797S, L858R/T790/C797S, Del19/C797S, and L858R/C797S. In vitro kinase assay and cellular assays showed high potency and selectivity. In vivo PK/PD and efficacy tests confirmed the great therapeutic potential of this inhibitor for patients with EGFR mutations. Citation Format: Dongsu Kim, Woo Seung Son, Anna Jang, Yeri Lee, Donggeon Kim, Changyu Choi, Kyung Hoon Min, Sung Pil Choi, Sang Kyun Lim. Discovery of a small-molecule inhibitor that can target EGFR with C797S mutation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 3323.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2022-3323
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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