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  1. Article ; Online: Rational strategies for enhancing mAb binding to SARS-CoV-2 variants through CDR diversification and antibody-escape prediction.

    Shah, Masaud / Shin, Ji-Yon / Woo, Hyun Goo

    Frontiers in immunology

    2023  Volume 14, Page(s) 1113175

    Abstract: Since the emergence of SARS-CoV-2, dozens of variants of interest and half a dozen variants of concern (VOCs) have been documented by the World Health Organization. The emergence of these VOCs due to the continuous evolution of the virus is a major ... ...

    Abstract Since the emergence of SARS-CoV-2, dozens of variants of interest and half a dozen variants of concern (VOCs) have been documented by the World Health Organization. The emergence of these VOCs due to the continuous evolution of the virus is a major concern for COVID-19 therapeutic antibodies and vaccines because they are designed to target prototype/previous strains and lose effectiveness against new VOCs. Therefore, there is a need for time- and cost-effective strategies to estimate the immune escape and redirect therapeutic antibodies against newly emerging variants. Here, we computationally predicted the neutralization escape of the SARS-CoV-2 Delta and Omicron variants against the mutational space of RBD-mAbs interfaces. Leveraging knowledge of the existing RBD-mAb interfaces and mutational space, we fine-tuned and redirected CT-p59 (Regdanvimab) and Etesevimab against the escaped variants through complementarity-determining regions (CDRs) diversification. We identified antibodies against the Omicron lineage BA.1 and BA.2 and Delta variants with comparable or better binding affinities to that of prototype Spike. This suggests that CDRs diversification by hotspot grafting, given an existing insight into the Ag-Abs interface, is an exquisite strategy to redirect antibodies against preselected epitopes and combat the neutralization escape of emerging SARS-CoV-2 variants.
    MeSH term(s) Humans ; SARS-CoV-2/genetics ; COVID-19 ; Antibodies, Monoclonal/therapeutic use ; Complementarity Determining Regions/genetics
    Chemical Substances Antibodies, Monoclonal ; Complementarity Determining Regions
    Language English
    Publishing date 2023-03-31
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1113175
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Src is essential for the endosomal delivery of the FGFR4 signaling complex in hepatocellular carcinoma.

    Shin, Ji-Yon / Ahn, Sung-Min

    Journal of translational medicine

    2021  Volume 19, Issue 1, Page(s) 138

    Abstract: Background: Hepatocytes usually express fibroblast growth factor receptor 4 (FGFR4), but not its ligand, fibroblast growth factor 19 (FGF19). A subtype of hepatocellular carcinoma (HCC) expresses FGF19, which activates the FGFR4 signaling pathway that ... ...

    Abstract Background: Hepatocytes usually express fibroblast growth factor receptor 4 (FGFR4), but not its ligand, fibroblast growth factor 19 (FGF19). A subtype of hepatocellular carcinoma (HCC) expresses FGF19, which activates the FGFR4 signaling pathway that induces cell proliferation. FGFR4 inhibitors that target this mechanism are under clinical development for the treatment of HCCs with FGF19 amplification or FGFR4 overexpression. Src plays an essential role in the FGFR1 and FGFR2 signaling pathways. However, it is yet to be understood whether Src has any role in the FGF19-FGFR4 pathway in HCCs. In this study, we aimed to elucidate the role of Src in the FGF19-FGFR4 axis in HCC.
    Methods: 3 HCC cell lines expressing both FGF19 and FGFR4 were selected. The expression of each protein was suppressed by siRNA treatment, and the activity-regulating relationship between FGFR4 and Src was investigated by westernblot. Co-immunoprecipitation was performed using the FGFR4 antibody to identify the endosomal complex formation and receptor endocytosis. The intracellular migration pathways of the endosomal complex were observed by immuno-fluorescence and nuclear co-immunoprecipitation. Dasatinib and BLU9931 were used for cytotoxicity comparison.
    Results: FGFR4 modulates the activity of Src and Src modulates the expression of FGFR4, showing a mutual regulatory relationship. FGFR4 activated by FGF19 formed an endosomal complex with Src and STAT3 and moved to the nucleus. However, when Src was suppressed, the formation of the endosomal complex was not observed. FGFR4 was released from the complex transferred into the nucleus and the binding of Src and STAT3 was maintained. Dasatinib showed cytotoxic results comparable to BLU9931. The results of our study demonstrated that Src is essential for the nuclear transport of STAT3, as it induces the endosomal delivery of FGFR4 in FGF19-expressing HCC cell lines.
    Conclusions: We found that Src is essential for the endosomal delivery of the FGFR4 signaling complex in HCC. Our findings provide a scientific rationale for repurposing Src inhibitors for the treatment of HCCs in which the FGFR4 pathway is activated.
    MeSH term(s) Carcinoma, Hepatocellular/drug therapy ; Cell Proliferation ; Fibroblast Growth Factors ; Humans ; Liver Neoplasms/drug therapy ; Receptor, Fibroblast Growth Factor, Type 4/metabolism ; Signal Transduction
    Chemical Substances Fibroblast Growth Factors (62031-54-3) ; FGFR4 protein, human (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 4 (EC 2.7.10.1)
    Language English
    Publishing date 2021-04-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1479-5876
    ISSN (online) 1479-5876
    DOI 10.1186/s12967-021-02807-4
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  3. Article ; Online: Characterization of HLA-A*33:03 epitopes via immunoprecipitation and LC-MS/MS.

    Khan, Amir / Shin, Ji-Yon / So, Min Kyung / Na, Jung-Hyun / Justesen, Sune / Ansari, Adnan Ahmad / Ko, Byoung Joon / Ahn, Sung-Min

    Proteomics

    2021  Volume 22, Issue 1-2, Page(s) e2100171

    Abstract: Human leukocyte antigen (HLA) class I has more than 18,000 alleles, each of which binds to a set of unique peptides from the cellular degradome. Deciphering the interaction between antigenic peptides and HLA proteins is crucial for understanding immune ... ...

    Abstract Human leukocyte antigen (HLA) class I has more than 18,000 alleles, each of which binds to a set of unique peptides from the cellular degradome. Deciphering the interaction between antigenic peptides and HLA proteins is crucial for understanding immune responses in autoimmune diseases and cancer. In this study, we aimed to characterize the peptidome that binds to HLA-A*33:03, which is one of the most prevalent HLA-A alleles in the Northeast Asian population, but poorly studied. For this purpose, we analyzed the HLA-A*33:03 monoallelic B cell line using immunoprecipitation of HLA-A and peptide complexes, followed by liquid chromatography-tandem mass spectrometry (LC-MS/MS). In this study, we identified 5731 unique peptides that were associated with HLA A*33:03, and experimentally validated the affinity of 40 peptides for HLA-A*33:03 and their stability in HLA A*33:03-peptides complexes. To our knowledge, this study represents the largest dataset of peptides associated with HLA-A*33:03. Also, this is the first study in which HLA A*33:03-associated peptides were experimentally validated.
    MeSH term(s) Chromatography, Liquid ; Epitopes ; HLA-A Antigens ; Humans ; Immunoprecipitation ; Tandem Mass Spectrometry
    Chemical Substances Epitopes ; HLA-A Antigens
    Language English
    Publishing date 2021-10-05
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2032093-0
    ISSN 1615-9861 ; 1615-9853
    ISSN (online) 1615-9861
    ISSN 1615-9853
    DOI 10.1002/pmic.202100171
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    Zs.A 5386: Show issues Location:
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  4. Article ; Online: Effect of the combination of metformin and fenofibrate on glucose homeostasis in diabetic Goto-Kakizaki rats.

    Oh, Tae Jung / Shin, Ji Yon / Kang, Gyeong Hoon / Park, Kyong Soo / Cho, Young Min

    Experimental & molecular medicine

    2013  Volume 45, Page(s) e30

    Abstract: Metformin has been reported to increase the expression of the glucagon-like peptide-1 (GLP-1) receptor in pancreatic beta cells in a peroxisome proliferator-activated receptor (PPAR)-α-dependent manner. We investigated whether a PPARα agonist, ... ...

    Abstract Metformin has been reported to increase the expression of the glucagon-like peptide-1 (GLP-1) receptor in pancreatic beta cells in a peroxisome proliferator-activated receptor (PPAR)-α-dependent manner. We investigated whether a PPARα agonist, fenofibrate, exhibits an additive or synergistic effect on glucose metabolism, independent of its lipid-lowering effect, when added to metformin. Non-obese diabetic Goto-Kakizaki (GK) rats were divided into four groups and treated for 28 days with metformin, fenofibrate, metformin plus fenofibrate or vehicle. The random blood glucose levels, body weights, food intake and serum lipid profiles were not significantly different among the groups. After 4 weeks, metformin, but not fenofibrate, markedly reduced the blood glucose levels during oral glucose tolerance tests, and this effect was attenuated by adding fenofibrate. Metformin increased the expression of the GLP-1 receptor in pancreatic islets, whereas fenofibrate did not. During the intraperitoneal glucose tolerance tests with the injection of a GLP-1 analog, metformin and/or fenofibrate did not alter the insulin secretory responses. In conclusion, fenofibrate did not confer any beneficial effect on glucose homeostasis but reduced metformin's glucose-lowering activity in GK rats, thus discouraging the addition of fenofibrate to metformin to improve glycemic control.
    MeSH term(s) Animals ; Blood Glucose/metabolism ; Body Weight/drug effects ; Diabetes Mellitus, Experimental/drug therapy ; Diabetes Mellitus, Experimental/metabolism ; Drug Therapy, Combination ; Exenatide ; Feeding Behavior/drug effects ; Fenofibrate/pharmacology ; Fenofibrate/therapeutic use ; Glucagon-Like Peptide 1/agonists ; Glucagon-Like Peptide 1/metabolism ; Glucagon-Like Peptide-1 Receptor ; Glucose/metabolism ; Glucose Tolerance Test ; Homeostasis/drug effects ; Immunohistochemistry ; Injections, Intraperitoneal ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/pathology ; Lipid Metabolism/drug effects ; Male ; Metformin/pharmacology ; Metformin/therapeutic use ; Peptides/administration & dosage ; Peptides/pharmacology ; Rats ; Receptors, Glucagon/metabolism ; Venoms/administration & dosage ; Venoms/pharmacology
    Chemical Substances Blood Glucose ; Glp1r protein, rat ; Glucagon-Like Peptide-1 Receptor ; Peptides ; Receptors, Glucagon ; Venoms ; Glucagon-Like Peptide 1 (89750-14-1) ; Metformin (9100L32L2N) ; Exenatide (9P1872D4OL) ; Glucose (IY9XDZ35W2) ; Fenofibrate (U202363UOS)
    Language English
    Publishing date 2013-07-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1328915-9
    ISSN 2092-6413 ; 1226-3613 ; 0378-8512
    ISSN (online) 2092-6413
    ISSN 1226-3613 ; 0378-8512
    DOI 10.1038/emm.2013.58
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    Zs.A 4775: Show issues Location:
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  5. Article: Anti-Cancer Effect of Ginsenoside F2 against Glioblastoma Multiforme in Xenograft Model in SD Rats.

    Shin, Ji Yon / Lee, Jung Min / Shin, Heon Sub / Park, Sang Yong / Yang, Jung Eun / Cho, Somi Kim / Yi, Tae-Hoo

    Journal of ginseng research

    2013  Volume 36, Issue 1, Page(s) 86–92

    Abstract: The glioblastoma multiforme (GBM) is the most common malignant brain tumor in adults. Despite combination treatments of radiation and chemotherapy, the survival periods are very short. Therefore, this study was conducted to assess the potential of ... ...

    Abstract The glioblastoma multiforme (GBM) is the most common malignant brain tumor in adults. Despite combination treatments of radiation and chemotherapy, the survival periods are very short. Therefore, this study was conducted to assess the potential of ginsenoside F2 (F2) to treat GBM. In in vitro experiments with glioblastoma cells U373MG, F2 showed the cytotoxic effect with IC50 of 50 μg/mL through apoptosis, confirmed by DNA condensation and fragmentation. The cell population of cell cycle sub-G1 as indicative of apoptosis was also increased. In xenograft model in SD rats, F2 at dosage of 35 mg/kg weight was intravenously injected every two days. This reduced the tumor growth in magnetic resonance imaging images. The immunohistochemistry revealed that the anticancer activity might be mediated through inhibition of proliferation judged by Ki67 and apoptosis induced by activation of caspase-3 and -8. And the lowered expression of CD31 showed the reduction in blood vessel densities. The expression of matrix metalloproteinase-9 for invasion of cancer was also inhibited. The cell populations with cancer stem cell markers of CD133 and nestin were reduced. The results of this study suggested that F2 could be a new potential chemotherapeutic drug for GBM treatment by inhibiting the growth and invasion of cancer.
    Language English
    Publishing date 2013-05-10
    Publishing country Korea (South)
    Document type Journal Article
    ZDB-ID 2765273-7
    ISSN 2093-4947 ; 1226-8453
    ISSN (online) 2093-4947
    ISSN 1226-8453
    DOI 10.5142/jgr.2012.36.1.86
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  6. Article ; Online: The incretin effect in Korean subjects with normal glucose tolerance or type 2 diabetes.

    Oh, Tae Jung / Kim, Min Young / Shin, Ji Yon / Lee, Jung Chan / Kim, Sungwan / Park, Kyong Soo / Cho, Young Min

    Clinical endocrinology

    2013  Volume 80, Issue 2, Page(s) 221–227

    Abstract: Background: The incretin effect is known to be decreased in type 2 diabetes. However, there are limited data on the incretin effect in non-Caucasian subjects. Because Asian patients with type 2 diabetes are characterized by decreased insulin secretion, ... ...

    Abstract Background: The incretin effect is known to be decreased in type 2 diabetes. However, there are limited data on the incretin effect in non-Caucasian subjects. Because Asian patients with type 2 diabetes are characterized by decreased insulin secretion, this study set out to examine the incretin effect in Korean subjects with normal glucose tolerance (NGT) or type 2 diabetes.
    Methods: We performed 75-g oral glucose tolerance tests (OGTTs) and corresponding isoglycaemic intravenous glucose infusion (IIGI) studies in Korean subjects with NGT (n = 14) or type 2 diabetes (n = 16). The incretin effect was calculated based on the incremental area under the curves (iAUCs) of the plasma levels of insulin, C-peptide or insulin secretion rate (ISR). The plasma levels of total glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) were measured by ELISA.
    Results: The incretin effect was not different between the subjects with NGT and type 2 diabetes (43 ± 6% vs 47 ± 4%, P = 0·575 by insulin; 29 ± 7% vs 38 ± 4%, P = 0·253 by C-peptide; 28 ± 7% vs 35 ± 5%, P = 0·372 by ISR, respectively). However, the gastrointestinally mediated glucose disposal (GIGD) was markedly decreased in type 2 diabetes (28·5 ± 4·2% vs 59·0 ± 4·3%, P < 0·001). The plasma levels of the total GLP-1 and GIP during the OGTTs were comparable between the two groups.
    Conclusion: In Koreans, the secretion of GLP-1 or GIP during OGTTs and the incretin effect were comparable between subjects with NGT and type 2 diabetes, whereas the GIGD was significantly decreased in patients with type 2 diabetes.
    MeSH term(s) Adult ; Asian Continental Ancestry Group ; Blood Glucose/metabolism ; C-Peptide/blood ; Diabetes Mellitus, Type 2/blood ; Diabetes Mellitus, Type 2/ethnology ; Gastric Inhibitory Polypeptide/blood ; Glucagon/blood ; Glucagon-Like Peptide 1/blood ; Glucose Tolerance Test ; Humans ; Incretins/blood ; Insulin/blood ; Insulin/metabolism ; Insulin Secretion ; Male ; Middle Aged ; Republic of Korea
    Chemical Substances Blood Glucose ; C-Peptide ; Incretins ; Insulin ; Gastric Inhibitory Polypeptide (59392-49-3) ; Glucagon-Like Peptide 1 (89750-14-1) ; Glucagon (9007-92-5)
    Language English
    Publishing date 2013-05-20
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 121745-8
    ISSN 1365-2265 ; 0300-0664
    ISSN (online) 1365-2265
    ISSN 0300-0664
    DOI 10.1111/cen.12167
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