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  1. Article ; Online: Single-cell multiomics

    Jeongwoo Lee / Do Young Hyeon / Daehee Hwang

    Experimental and Molecular Medicine, Vol 52, Iss 9, Pp 1428-

    technologies and data analysis methods

    2020  Volume 1442

    Abstract: Single-cell profiling: understanding disease at the cellular level The expansion of single-cell profiling technologies will provide unprecedented insights into the molecular mechanisms inherent in disease. Novel technologies known collectively as ‘single- ...

    Abstract Single-cell profiling: understanding disease at the cellular level The expansion of single-cell profiling technologies will provide unprecedented insights into the molecular mechanisms inherent in disease. Novel technologies known collectively as ‘single-cell multiomics’ enable systematic, high-resolution profiling of DNA, RNA and proteins in individual cells. This provides valuable data about gene regulation and molecular populations, and cellular processes during disease development and progression. Daehee Hwang and co-workers at Seoul National University, Seoul, South Korea, reviewed existing single-cell multiomics technologies and highlighted ways to integrate the data generated. Analytical features of multiomics allow scientists to isolate, sequence and label (or ‘barcode’) multiple molecules in single cells. Different sequencing techniques can be used for different purposes, such as exploring gene mutation coverage or measuring RNA transcripts. Combining these sequencing data will help identify links between significant features during disease.
    Keywords Medicine ; R ; Biochemistry ; QD415-436
    Subject code 612
    Language English
    Publishing date 2020-09-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: DNA repair and cholesterol-mediated drug efflux induce dose-dependent chemoresistance in nutrient-deprived neuroblastoma cells

    Soo Yeon Chae / Dowoon Nam / Do Young Hyeon / Areum Hong / Timothy Dain Lee / Sujin Kim / Dongjoon Im / Jiwon Hong / Chaewon Kang / Ji Won Lee / Daehee Hwang / Sang-Won Lee / Hugh I. Kim

    iScience, Vol 24, Iss 4, Pp 102325- (2021)

    2021  

    Abstract: Summary: Neuroblastoma is a solid, heterogeneous pediatric tumor. Chemotherapy is widely used to treat neuroblastoma. However, dose-dependent responses and chemoresistance mechanisms of neuroblastoma cells to anticancer drugs remain challenging. Here, we ...

    Abstract Summary: Neuroblastoma is a solid, heterogeneous pediatric tumor. Chemotherapy is widely used to treat neuroblastoma. However, dose-dependent responses and chemoresistance mechanisms of neuroblastoma cells to anticancer drugs remain challenging. Here, we investigated the dose-dependent effects of topotecan on human neuroblastoma cells (SK-N-SH, SH-SY5Y, and SK-N-BE) under various nutrient supply conditions. Serum-starved human neuroblastoma cells showed reduced toxicity. Their survival rate increased upon treatment with a high concentration (1 μM) of topotecan. Quantitative profiling of global and phosphoproteome identified 12,959 proteins and 48,812 phosphosites, respectively, from SK-N-SH cells. Network analysis revealed that topotecan upregulated DNA repair and cholesterol-mediated topotecan efflux, resulting in topotecan resistance. Results of DNA damage assay, cell cycle, and quantitative analyses of membrane cholesterol supported the validity of these resistance factors and their applicability to all neuroblastoma cells. Our results provide a model for high dose-dependent chemoresistance in neuroblastoma cells that could enable a patient-dependent chemotherapy screening strategy.
    Keywords Molecular Biology ; Cancer ; Proteomics ; Science ; Q
    Language English
    Publishing date 2021-04-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Integrative analysis of transcriptomic data for identification of T-cell activation-related mRNA signatures indicative of preterm birth

    Jae Young Yoo / Do Young Hyeon / Yourae Shin / Soo Min Kim / Young-Ah You / Daye Kim / Daehee Hwang / Young Ju Kim

    Scientific Reports, Vol 11, Iss 1, Pp 1-

    2021  Volume 12

    Abstract: Abstract Preterm birth (PTB), defined as birth at less than 37 weeks of gestation, is a major determinant of neonatal mortality and morbidity. Early diagnosis of PTB risk followed by protective interventions are essential to reduce adverse neonatal ... ...

    Abstract Abstract Preterm birth (PTB), defined as birth at less than 37 weeks of gestation, is a major determinant of neonatal mortality and morbidity. Early diagnosis of PTB risk followed by protective interventions are essential to reduce adverse neonatal outcomes. However, due to the redundant nature of the clinical conditions with other diseases, PTB-associated clinical parameters are poor predictors of PTB. To identify molecular signatures predictive of PTB with high accuracy, we performed mRNA sequencing analysis of PTB patients and full-term birth (FTB) controls in Korean population and identified differentially expressed genes (DEGs) as well as cellular pathways represented by the DEGs between PTB and FTB. By integrating the gene expression profiles of different ethnic groups from previous studies, we identified the core T-cell activation pathway associated with PTB, which was shared among all previous datasets, and selected three representative DEGs (CYLD, TFRC, and RIPK2) from the core pathway as mRNA signatures predictive of PTB. We confirmed the dysregulation of the candidate predictors and the core T-cell activation pathway in an independent cohort. Our results suggest that CYLD, TFRC, and RIPK2 are potentially reliable predictors for PTB.
    Keywords Medicine ; R ; Science ; Q
    Subject code 610
    Language English
    Publishing date 2021-01-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: CCN1 interlinks integrin and hippo pathway to autoregulate tip cell activity

    Myo-Hyeon Park / Ae kyung Kim / Sarala Manandhar / Su-Young Oh / Gun-Hyuk Jang / Li Kang / Dong-Won Lee / Do Young Hyeon / Sun-Hee Lee / Hye Eun Lee / Tae-Lin Huh / Sang Heon Suh / Daehee Hwang / Kyunghee Byun / Hae-Chul Park / You Mie Lee

    eLife, Vol

    2019  Volume 8

    Abstract: CCN1 (CYR61) stimulates active angiogenesis in various tumours, although the mechanism is largely unknown. Here, we report that CCN1 is a key regulator of endothelial tip cell activity in angiogenesis. Microvessel networks and directional vascular cell ... ...

    Abstract CCN1 (CYR61) stimulates active angiogenesis in various tumours, although the mechanism is largely unknown. Here, we report that CCN1 is a key regulator of endothelial tip cell activity in angiogenesis. Microvessel networks and directional vascular cell migration patterns were deformed in ccn1-knockdown zebrafish embryos. CCN1 activated VEGFR2 and downstream MAPK/PI3K signalling pathways, YAP/TAZ, as well as Rho effector mDia1 to enhance tip cell activity and CCN1 itself. VEGFR2 interacted with integrin αvβ3 through CCN1. Integrin αvβ3 inhibitor repressed tip cell number and sprouting in postnatal retinas from endothelial cell-specific Ccn1 transgenic mice, and allograft tumours in Ccn1 transgenic mice showed hyperactive vascular sprouting. Cancer patients with high CCN1 expression have poor survival outcomes and positive correlation with ITGAV and ITGB3 and high YAP/WWTR1. Thus, our data underscore the positive feedback regulation of tip cells by CCN1 through integrin αvβ3/VEGFR2 and increased YAP/TAZ activity, suggesting a promising therapeutic intervention for pathological angiogenesis.
    Keywords Cyr61 ; integrinαvβ3 ; VEGFR2 ; YAP/TAZ ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
    Subject code 571
    Language English
    Publishing date 2019-08-01T00:00:00Z
    Publisher eLife Sciences Publications Ltd
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Golgi Outpost Synthesis Impaired by Toxic Polyglutamine Proteins Contributes to Dendritic Pathology in Neurons

    Chang Geon Chung / Min Jee Kwon / Keun Hye Jeon / Do Young Hyeon / Myeong Hoon Han / Jeong Hyang Park / In Jun Cha / Jae Ho Cho / Kunhyung Kim / Sangchul Rho / Gyu Ree Kim / Hyobin Jeong / Jae Won Lee / TaeSoo Kim / Keetae Kim / Kwang Pyo Kim / Michael D. Ehlers / Daehee Hwang / Sung Bae Lee

    Cell Reports, Vol 20, Iss 2, Pp 356-

    2017  Volume 369

    Abstract: Dendrite aberration is a common feature of neurodegenerative diseases caused by protein toxicity, but the underlying mechanisms remain largely elusive. Here, we show that nuclear polyglutamine (polyQ) toxicity resulted in defective terminal dendrite ... ...

    Abstract Dendrite aberration is a common feature of neurodegenerative diseases caused by protein toxicity, but the underlying mechanisms remain largely elusive. Here, we show that nuclear polyglutamine (polyQ) toxicity resulted in defective terminal dendrite elongation accompanied by a loss of Golgi outposts (GOPs) and a decreased supply of plasma membrane (PM) in Drosophila class IV dendritic arborization (da) (C4 da) neurons. mRNA sequencing revealed that genes downregulated by polyQ proteins included many secretory pathway-related genes, including COPII genes regulating GOP synthesis. Transcription factor enrichment analysis identified CREB3L1/CrebA, which regulates COPII gene expression. CrebA overexpression in C4 da neurons restores the dysregulation of COPII genes, GOP synthesis, and PM supply. Chromatin immunoprecipitation (ChIP)-PCR revealed that CrebA expression is regulated by CREB-binding protein (CBP), which is sequestered by polyQ proteins. Furthermore, co-overexpression of CrebA and Rac1 synergistically restores the polyQ-induced dendrite pathology. Collectively, our results suggest that GOPs impaired by polyQ proteins contribute to dendrite pathology through the CBP-CrebA-COPII pathway.
    Keywords polyQ ; Golgi outposts ; CrebA ; CREB3L1 ; CBP ; dendrites ; neurodegeneration ; ataxin-3 ; nuclear proteotoxicity ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2017-07-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article: The Arabidopsis NAC Transcription Factor ANAC096 Cooperates with bZIP-Type Transcription Factors in Dehydration and Osmotic Stress Responses

    Xu, Zheng-Yi / Dae Heon Kim / Daehee Hwang / Do Young Hyeon / Inhwan Hwang / Jing Bo Jin / Jong Chan Hong / Se-Hwan Joo / Seong-Ki Kim / Soo Youn Kim / Ting Dong / Youngmin Park

    plant cell. 2013 Nov., v. 25, no. 11

    2013  

    Abstract: This work examines the role of the NAC transcription factor ANAC096, finding that ANAC096 interacts with specific bZIP transcription factors to globally affect abscisic acid–responsive transcription during osmotic and drought stresses. ...

    Abstract This work examines the role of the NAC transcription factor ANAC096, finding that ANAC096 interacts with specific bZIP transcription factors to globally affect abscisic acid–responsive transcription during osmotic and drought stresses.
    Keywords Arabidopsis ; basic-leucine zipper transcription factors ; drought ; osmotic stress ; osmotic treatment ; stress response
    Language English
    Dates of publication 2013-11
    Size p. 4708-4724.
    Publishing place American Society of Plant Biologists
    Document type Article
    ZDB-ID 623171-8
    ISSN 1532-298X ; 1040-4651
    ISSN (online) 1532-298X
    ISSN 1040-4651
    DOI 10.1105/tpc.113.119099
    Database NAL-Catalogue (AGRICOLA)

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