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5 results on '"Grace Sanghee Lee"'

1. Cell Culture Systems for Studying Hepatitis B and Hepatitis D Virus Infections

Author

Grace Sanghee Lee, Michael A. Purdy, and Youkyung Choi

Subjects
hepatitis B virus (HBV), hepatitis D virus (HDV), cell culture systems, co-infection and super-infection HBV/HDV, Science
Abstract

The hepatitis B virus (HBV) and hepatitis D virus (HDV) infections cause liver disease, including hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). HBV infection remains a major global health problem. In 2019, 296 million people were living with chronic hepatitis B and about 5% of them were co-infected with HDV. In vitro cell culture systems are instrumental in the development of therapeutic targets. Cell culture systems contribute to identifying molecular mechanisms for HBV and HDV propagation, finding drug targets for antiviral therapies, and testing antiviral agents. Current HBV therapeutics, such as nucleoside analogs, effectively suppress viral replication but are not curative. Additionally, no effective treatment for HDV infection is currently available. Therefore, there is an urgent need to develop therapies to treat both viral infections. A robust in vitro cell culture system supporting HBV and HDV infections (HBV/HDV) is a critical prerequisite to studying HBV/HDV pathogenesis, the complete life cycle of HBV/HDV infections, and consequently identifying new therapeutics. However, the lack of an efficient cell culture system hampers the development of novel antiviral strategies for HBV/HDV infections. In vitro cell culture models have evolved with significant improvements over several decades. Recently, the development of the HepG2-NTCP sec+ cell line, expressing the sodium taurocholate co-transporting polypeptide receptor (NTCP) and self-assembling co-cultured primary human hepatocytes (SACC-PHHs) has opened new perspectives for a better understanding of HBV and HDV lifecycles and the development of specific antiviral drug targets against HBV/HDV infections. We address various cell culture systems along with different cell lines and how these cell culture systems can be used to provide better tools for HBV and HDV studies. more...

Published
2023
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3. Mispair-bound human MutS–MutL complex triggers DNA incisions and activates mismatch repair

Author

Guo Min Li, Wei Yang, Grace Sanghee Lee, Liya Gu, and Janice Ortega

Subjects
Adenosine Triphosphatases, congenital, hereditary, and neonatal diseases and abnormalities, Nuclease, DNA Repair, biology, Base Pair Mismatch, DNA, Cell Biology, DNA Mismatch Repair, MutS DNA Mismatch-Binding Protein, Article, Cell biology, DNA-Binding Proteins, Exonuclease 1, chemistry.chemical_compound, chemistry, biology.protein, Humans, DNA mismatch repair, Molecular Biology
Abstract

DNA mismatch repair (MMR) relies on MutS and MutL ATPases for mismatch recognition and strand-specific nuclease recruitment to remove mispaired bases in daughter strands. However, whether the MutS–MutL complex coordinates MMR by ATP-dependent sliding on DNA or protein–protein interactions between the mismatch and strand discrimination signal is ambiguous. Using functional MMR assays and systems preventing proteins from sliding, we show that sliding of human MutSα is required not for MMR initiation, but for final mismatch removal. MutSα recruits MutLα to form a mismatch-bound complex, which initiates MMR by nicking the daughter strand 5′ to the mismatch. Exonuclease 1 (Exo1) is then recruited to the nick and conducts 5′ → 3′ excision. ATP-dependent MutSα dissociation from the mismatch is necessary for Exo1 to remove the mispaired base when the excision reaches the mismatch. Therefore, our study has resolved a long-standing puzzle, and provided new insights into the mechanism of MMR initiation and mispair removal. more...

Published
2021
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4. Author Correction: Identification of novel genetic variants predisposing to familial oral squamous cell carcinomas

Author

Jizhi Zhao, Grace Sanghee Lee, Jia Zhang, Guo Min Li, Guogen Mao, Yaping Huang, Liya Gu, Lijun Bi, Joseph Valentino, and Zhijie Chang

Subjects
lcsh:Cytology, Oral cancer, Cell, Genetic variants, MEDLINE, Oncogenes, Cell Biology, Computational biology, Biology, Biochemistry, Article, stomatognathic diseases, medicine.anatomical_structure, Cancer genetics, Genetics, medicine, Identification (biology), lcsh:QH573-671, Molecular Biology
Abstract

Oral squamous cell carcinoma (OSCC) is a common subtype of head and neck squamous cell carcinoma (HNSCC), but the pathogenesis underlying familial OSCCs is unknown. Here, we analyzed whole-genome sequences of a family with autosomal dominant expression of oral tongue cancer and identified proto-oncogenes VAV2 and IQGAP1 as the primary factors responsible for oral cancer in the family. These two genes are also frequently mutated in sporadic OSCCs and HNSCCs. Functional analysis revealed that the detrimental variants target tumorigenesis-associated pathways, thus confirming that these novel genetic variants help to establish a predisposition to familial OSCC. more...

Published
2020
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5. Identification of novel genetic variants predisposing to familial oral squamous cell carcinomas

Author

Lijun Bi, Guogen Mao, Liya Gu, Jizhi Zhao, Yaping Huang, Zhijie Chang, Guo Min Li, Grace Sanghee Lee, Joseph Valentino, and Jia Zhang

Subjects
lcsh:Cytology, Oral cancer, Cell, Cancer, Correction, Cell Biology, Oncogenes, Biology, medicine.disease, Biochemistry, Head and neck squamous-cell carcinoma, Pathogenesis, stomatognathic diseases, medicine.anatomical_structure, IQGAP1, Tongue, Genetics, medicine, Cancer research, Identification (biology), lcsh:QH573-671, Molecular Biology, Gene, Cancer genetics
Abstract

Oral squamous cell carcinoma (OSCC) is a common subtype of head and neck squamous cell carcinoma (HNSCC), but the pathogenesis underlying familial OSCCs is unknown. Here, we analyzed whole-genome sequences of a family with autosomal dominant expression of oral tongue cancer and identified proto-oncogenes VAV2 and IQGAP1 as the primary factors responsible for oral cancer in the family. These two genes are also frequently mutated in sporadic OSCCs and HNSCCs. Functional analysis revealed that the detrimental variants target tumorigenesis-associated pathways, thus confirming that these novel genetic variants help to establish a predisposition to familial OSCC. more...

Published
2019