國立陽明交通大學工程生物科學院徵聘教師啟事

國立陽明交通大學工程生物科學院徵聘教師啟事

 

  • 工程生物科學院(原生物科技學院,下稱本院)由生物科技學系、分子醫學與生物工程研究所、生物資訊及系統生物研究所組成,本院以工程生物科學(Engineering Bioscience)從分子層次鏈結生物科技、ICT與計算生物,發展精準醫藥、轉譯工程及永續科技等領域,以建立健康、幸福、及永續的未來。本院在陽明交通大學立足於化學、物理、工程等尖端科技與生物科學的界面,以跨領域模式聯通基礎科學與產業應用,在生物電子、生物資訊、生醫材料、組織工程、微生物工程、合成生物、結構生物、與神經科技等領域成果豐碩。

  • 師資需求名額:數名。

  • Faculty positions available: Professor, Associate Professor, and Assistant Professor

  • Application requirements:

  • 強烈認同本院發展理念與願景,對卓越研究與教學有熱情之生物科技與工程相關領域人才(包含但不限於生物電子、生醫材料、類器官與組織工程、細胞治療、生物大數據AI、計算生物、計算化學、代謝體學、微生物基因體學、合成生物、分子生醫影像、結構生物、永續科技、智慧醫療)皆歡迎申請。

  • 應徵人需有上述或相關領域博士學位

  • Additional Requirements: Successful candidates will be required to teach courses in English for the first three years of his or her appointment.

  • 應徵截止日期:應徵資料將於2023/12/05截止收件

  • Application package should include:

          (1)應徵意願書(Cover Letter)

         (2)Curriculum Vitae

         (3)著作清單及代表性論文抽印本

        (4)研究及教學計畫書

        (5)Three reference letters sent directly by external referees

        (6)Estimated laboratory start-up budget and instrumentation needs.

  • Please send the application package to:
    將上述資料以e-mail寄送至分子醫學與生物工程研究所黃兆祺所長並副本至郭淑卿小姐,相關聯絡資訊如下:

黃兆祺所長(hwangeric@nycu.edu.tw)
郭淑卿小姐(sunny@nycu.edu.tw)
Tel:+886-3-5712121轉56937 (郭小姐)
CBT hompage:https://cbt.nycu.edu.tw/

Molecular insight into the specific enzymatic properties of TREX1 revealing the diverse functions in processing RNA and DNA/RNA hybrids

蕭育源教授及朱智瑋教授研究團隊發表研究成果於Nucleic Acids Res

連結網址:https://pubmed.ncbi.nlm.nih.gov/37870446/

Abstract

In various autoimmune diseases, dysfunctional TREX1 (Three prime Repair Exonuclease 1) leads to accumulation of endogenous single-stranded DNA (ssDNA), double-stranded DNA (dsDNA) and DNA/RNA hybrids in the cytoplasm and triggers immune activation through the cGAS-STING pathway. Although inhibition of TREX1 could be a useful strategy for cancer immunotherapy, profiling cellular functions in terms of its potential substrates is a key step. Particularly important is the functionality of processing DNA/RNA hybrids and RNA substrates. The exonuclease activity measurements conducted here establish that TREX1 can digest both ssRNA and DNA/RNA hybrids but not dsRNA. The newly solved structures of TREX1-RNA product and TREX1-nucleotide complexes show that 2′-OH does not impose steric hindrance or specific interactions for the recognition of RNA. Through all-atom molecular dynamics simulations, we illustrate that the 2′-OH-mediated intra-chain hydrogen bonding in RNA would affect the binding with TREX1 and thereby reduce the exonuclease activity. This notion of higher conformational rigidity in RNA leading TREX1 to exhibit weaker catalytic cleavage is further validated by the binding affinity measurements with various synthetic DNA-RNA junctions. The results of this work thus provide new insights into the mechanism by which TREX1 processes RNA and DNA/RNA hybrids and contribute to the molecular-level understanding of the complex cellular functions of TREX1 as an exonuclease.

Single-Cell Meta-Analysis of Neutrophil Activation in Kawasaki Disease and Multisystem Inflammatory Syndrome in Children Reveals Potential Shared Immunological Drivers

柯泰名副教授研究團隊發表研究成果於Circulation

連結網址:https://www.ahajournals.org/doi/abs/10.1161/CIRCULATIONAHA.123.064734

Abstract

BACKGROUND:

Kawasaki disease (KD) and multisystem inflammatory syndrome in children (MIS-C) share similar clinical manifestations, including cardiovascular complications, suggesting similar underlying immunopathogenic processes. Aberrant neutrophil activation may play a crucial role in the shared pathologies of KD and MIS-C; however, the associated pathogenic mechanisms and molecular drivers remain unknown.

 

METHODS:

We performed a single-cell meta-analysis of neutrophil activation with 103 pediatric single-cell transcriptomic peripheral blood mononuclear cell data across 9 cohorts, including healthy controls, KD, MIS-C, compared with dengue virus infection, juvenile idiopathic arthritis, and pediatric celiac disease. We used a series of computational analyses to investigate the shared neutrophil transcriptional programs of KD and MIS-C that are linked to systemic damage and cardiac pathologies, and suggested Food and Drug Administration–approved drugs to consider as KD and MIS-C treatment.

 

RESULTS:

We meta-analyzed 521 950 high-quality cells. We found that blood signatures associated with risks of cardiovascular events are enriched in neutrophils of KD and MIS-C. We revealed the expansion of CD177+ neutrophils harboring hyperactivated effector functions in both KD and MIS-C, but not in healthy controls or in other viral-, inflammatory-, or immune-related pediatric diseases. KD and MIS-C CD177+ neutrophils had highly similar transcriptomes, marked by conserved signatures and pathways related to molecular damage. We found the induction of a shared neutrophil expression program, potentially regulated by SPI1 (Spi-1 proto-oncogene), which confers enhanced effector functions, especially neutrophil degranulation. CD177 and shared neutrophil expression program expressions were associated with acute stages and attenuated during KD intravenous immunoglobulin treatment and MIS-C recovery. Network analysis identified hub genes that correlated with the high activation of CD177+ neutrophils. Disease-gene association analysis revealed that the KD and MIS-C CD177+ neutrophils’ shared expression program was associated with the development of coronary and myocardial disorders. Last, we identified and validated TSPO (translocator protein) and S100A12 (S100 calcium-binding protein A12) as main molecular targets, for which the Food and Drug Administration–approved drugs methotrexate, zaleplon, metronidazole, lorazepam, clonazepam, temazepam, and zolpidem, among others, are primary candidates for drug repurposing.

 

CONCLUSIONS:

Our findings indicate that CD177+ neutrophils may exert systemic pathological damage contributing to the shared morbidities in KD and MIS-C. We uncovered potential regulatory drivers of CD177+ neutrophil hyperactivation and pathogenicity that may be targeted as a single therapeutic strategy for either KD or MIS-C.

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