The Genome Sequence Archive (GSA) is a data repository for archiving raw sequence data, which provides data storage and sharing services for worldwide scientific communities. Considering explosive data growth with diverse data types, here we present the GSA family by expanding into a set of resources for raw data archive with different purposes, namely, GSA (https://ngdc.cncb.ac.cn/gsa/), GSA for Human (GSA-Human, https://ngdc.cncb.ac.cn/gsa-human/), and Open Archive for Miscellaneous Data (OMIX, https://ngdc.cncb.ac.cn/omix/). Compared with the 2017 version, GSA has been significantly updated in data model, online functionalities, and web interfaces. GSA-Human, as a new partner of GSA, is a data repository specialized in human genetics-related data with controlled access and security. OMIX, as a critical complement to the two resources mentioned above, is an open archive for miscellaneous data. Together, all these resources form a family of resources dedicated to archiving explosive data with diverse types, accepting data submissions from all over the world, and providing free open access to all publicly available data in support of worldwide research activities.

Data Sharing

Data set

Data access

10.1016/j.gpb.2021.08.001

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Citations (974)

Supplementary Figure S1, S2, S3 from MACdb: A Curated Knowledgebase for Metabolic Associations across Human Cancers

Yanling Sun Xinchang Zheng Guoliang Wang Yibo Wang Xiaoning Chen

Supplementary Figure S1, S2, S3

10.1158/1541-7786.22700242.v1

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Citations (0)

Supplementary Table S1, S2 from MACdb: A Curated Knowledgebase for Metabolic Associations across Human Cancers

Yanling Sun Xinchang Zheng Guoliang Wang Yibo Wang Xiaoning Chen

Supplementary Table S1, S2

Table (database)

10.1158/1541-7786.22700236.v1

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Supplementary Table S1, S2 from MACdb: A Curated Knowledgebase for Metabolic Associations across Human Cancers

Yanling Sun Xinchang Zheng Guoliang Wang Yibo Wang Xiaoning Chen

Supplementary Table S1, S2

Table (database)

10.1158/1541-7786.22700236

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Supplementary Methods from MACdb: A Curated Knowledgebase for Metabolic Associations across Human Cancers

Yanling Sun Xinchang Zheng Guoliang Wang Yibo Wang Xiaoning Chen

Supplementary Methods

R package

10.1158/1541-7786.22700239.v1

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Influenza virus matrix protein M1 interacts with SLD5 to block host cell cycle

Cellular Microbiology (2019)

Li Zhu Wenming Zhao Jiao Lu Shan Li Kai Zhou

Influenza virus matrix 1 protein (M1) is highly conserved and plays essential roles at many stages of virus life cycle. Here, we used a yeast two-hybrid system to identify the host protein SLD5, a component of the GINS complex, which is essential for the initiation of DNA replication in eukaryotic cells, as a new M1 interacting protein. M1 from several different influenza virus strains all interacted with SLD5. Overexpression of SLD5 suppressed influenza virus replication. Transient, stable, or inducible expression of M1 induced host cell cycle blockade at G0/G1 phase. Moreover, SLD5 partially rescued M1 expression- or influenza virus infection-induced G0/G1 phase accumulation in cell lines and primary mouse embryonic fibroblasts. Importantly, SLD5 transgenic mice exhibited higher resistance and improved lung epithelial regeneration after virus infection compared with wild-type mice. Therefore, influenza virus M1 blocks host cell cycle process by interacting with SLD5. Our finding reveals the multifunctional nature of M1 and provides new insight for understanding influenza virus–host interaction.

Viral life cycle

VP40

10.1111/cmi.13038

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Citations (14)

Deaminase-Dead Mouse APOBEC3 Is an In Vivo Retroviral Restriction Factor

Journal of Virology (2018)

Spyridon Stavrou Wenming Zhao Kristin Blouch Susan R. Ross

The apolipoprotein B editing complex 3 (APOBEC3) proteins are potent retroviral restriction factors that are under strong positive selection, both in terms of gene copy number and sequence diversity. A common feature of all the members of the APOBEC3 family is the presence of one or two cytidine deamination domains, essential for cytidine deamination of retroviral reverse transcripts as well as packaging into virions. Several studies have indicated that human and mouse APOBEC3 proteins restrict retrovirus infection via cytidine deaminase (CD)-dependent and -independent means. To understand the relative contribution of CD-independent restriction in vivo, we created strains of transgenic mice on an APOBEC3 knockout background that express a deaminase-dead mouse APOBEC3 due to point mutations in both CD domains (E73Q/E253Q). Here, we show that the CD-dead APOBEC3 can restrict murine retroviruses in vivo Moreover, unlike the wild-type protein, the mutant APOBEC3 is not packaged into virions but acts only as a cell-intrinsic restriction factor that blocks reverse transcription by incoming viruses. Finally, we show that wild-type and CD-dead mouse APOBEC3 can bind to murine leukemia virus (MLV) reverse transcriptase. Our findings suggest that the mouse APOBEC3 cytidine deaminase activity is not required for retrovirus restriction.IMPORTANCE APOBEC3 proteins are important host cellular restriction factors essential for restricting retrovirus infection by causing mutations in the virus genome and by blocking reverse transcription. While both methods of restriction function in vitro, little is known about their role during in vivo infection. By developing transgenic mice with mutations in the cytidine deamination domains needed for enzymatic activity and interaction with viral RNA, we show that APOBEC3 proteins can still restrict in vivo infection by interacting with reverse transcriptase and blocking its activity. These studies demonstrate that APOBEC3 proteins have evolved multiple means for blocking retrovirus infection and that all of these means function in vivo.

Cytidine

APOBEC3G

10.1128/jvi.00168-18

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Global cold-chain related SARS-CoV-2 transmission identified by pandemic-scale phylogenomics

动物学研究 (2022)

Dalang Yu Junwei Zhu Jianing Yang Yi-Hsuan Pan Hailong Mu

Phylogenomics

Pandemic

2019-20 coronavirus outbreak

10.24272/j.issn.2095-8137.2022.238

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The Global Landscape of SARS-CoV-2 Genomes, Variants, and Haplotypes in 2019nCoVR

Genomics Proteomics & Bioinformatics (2020)

Shuhui Song Lina Ma Dong Zou Dongmei Tian Cuiping Li

Abstract On January 22, 2020, China National Center for Bioinformation (CNCB) released the 2019 Novel Coronavirus Resource (2019nCoVR), an open-access information resource for the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). 2019nCoVR features a comprehensive integration of sequence and clinical information for all publicly available SARS-CoV-2 isolates, which are manually curated with value-added annotations and quality evaluated by an automated in-house pipeline. Of particular note, 2019nCoVR offers systematic analyses to generate a dynamic landscape of SARS-CoV-2 genomic variations at a global scale. It provides all identified variants and their detailed statistics for each virus isolate, and congregates the quality score, functional annotation, and population frequency for each variant. Spatiotemporal change for each variant can be visualized and historical viral haplotype network maps for the course of the outbreak are also generated based on all complete and high-quality genomes available. Moreover, 2019nCoVR provides a full collection of SARS-CoV-2 relevant literature on the coronavirus disease 2019 (COVID-19), including published papers from PubMed as well as preprints from services such as bioRxiv and medRxiv through Europe PMC. Furthermore, by linking with relevant databases in CNCB, 2019nCoVR offers data submission services for raw sequence reads and assembled genomes, and data sharing with NCBI. Collectively, SARS-CoV-2 is updated daily to collect the latest information on genome sequences, variants, haplotypes, and literature for a timely reflection, making 2019nCoVR a valuable resource for the global research community. 2019nCoVR is accessible at https://bigd.big.ac.cn/ncov/.

2019-20 coronavirus outbreak

Pandemic

Coronavirus

10.1016/j.gpb.2020.09.001

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Citations (110)