Publications by authors named "Jingyuan Cong"

Article Synopsis
  • T-even type bacteriophages are important model organisms used to study biological processes like DNA topology regulation during replication, which is influenced by type IIA DNA topoisomerases.
  • This study reveals the cryo-EM structures of topoisomerase II from T4 and T6 phages, showcasing both apo and DNA-binding states, providing new insights into their mechanisms.
  • The research highlights unique interactions and functions of phage topoisomerase II, enhancing our understanding compared to prokaryotic and eukaryotic counterparts and featuring potential applications for developing inhibitors.
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Type II topoisomerases are ubiquitous enzymes that play a pivotal role in modulating the topological configuration of double-stranded DNA. These topoisomerases are required for DNA metabolism and have been extensively studied in both prokaryotic and eukaryotic organisms. However, our understanding of virus-encoded type II topoisomerases remains limited.

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Newcastle disease virus (NDV) belongs to Paramyxoviridae, which contains lethal human and animal pathogens. NDV RNA genome is replicated and transcribed by a multifunctional 250 kDa RNA-dependent RNA polymerase (L protein). To date, high-resolution structure of NDV L protein complexed with P protein remains to be elucidated, limiting our understanding of the molecular mechanisms of Paramyxoviridae replication/transcription.

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Human noroviruses (huNoVs) cause epidemic acute gastroenteritis using histo-blood group antigens (HBGAs) as host receptors or attachment factors to initiate an infection. While most huNoVs have been shown to bind HBGAs, some known clinical isolates, such as GI.3 DSV and VA115, do not recognize any HBGAs and thus the molecular mechanism behind their infections remains elusive.

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Junin virus (JUNV) causes Argentine hemorrhagic fever, a debilitating human disease of high mortality rates and a great risk to public health worldwide. Studying the L protein that replicates and transcribes the genome of JUNV, and its regulator Z protein should provide critical clues to identify therapeutic targets for disrupting the life cycle of JUNV. Here we report the 3.

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