Nucleocapsid mutations in SARS-CoV-2 augment replication and pathogenesis

NIAID Data Ecosystem2026-03-13 收录

突变体功能验证

SARS-CoV-2致病机理

数据链接：

https://www.ncbi.nlm.nih.gov/bioproject/PRJNA773399 数据链接链接失效反馈

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资源简介：

Raw sequencing data for cell culture and animal experiments of SARS-CoV-2 mutant competition assays

创建时间：

2021-10-21

Next Generation Sequencing Facilitates Quantitative Analysis of wild-type and erf4 mutant Transcriptomes

植物转录组分析

突变体功能验证

Analysis of gene expression level. The hypothesis tested in the present study was that erf4 mutant affects PMEI genes expression which inhibited PME activity in the seed coat mucilage Overall design:

NIAID Data Ecosystem60

irs4 versus CAI-12

基因表达谱分析

突变体功能验证

Comparison of expression profiling of irs4 null mutant versus isogenic strain (CAI-12) grown in blood (3 replicates) Two-condition experiment, irs4 null mutant versus CAI-12 wild-type. Biological repl

NIAID Data Ecosystem30

Expression data from yeast cells with pop2 deletion and overexpressing STM1 or STM1 R237K mutant

酵母基因表达

突变体功能验证

A880 has pop2 deletion and a very slow-growth phenotype with glycerol as carbon source. A880 transformed with 2-micron plasmids encoding STM1 can grow robustly on glycerol plates. The Arg237 on Stm1p

NIAID Data Ecosystem30

Identification of Germline Monoallelic Mutations in IKZF2 in Patients with Immune Dysregulation.

免疫遗传学

突变体功能验证

Helios, encoded by IKZF2, is a member of the Ikaros family of transcription factors with pivotal roles in T-follicular helper, NK- and T-regulatory cell physiology. Somatic IKZF2 mutations are frequen

NIAID Data Ecosystem30

The N121T and N121S substitutions on the spike protein of SARS-CoV-2 have a greater impact on serum neutralization reactions compared to biliverdin binding

突变体功能验证

血清尿酸

The N121 site on the spike N-terminal domain (NTD) of SARS-CoV-2 is known to be associated with heme and its metabolite, biliverdin, which can affect antibody binding. Either N121T or N121S substituti

NIAID Data Ecosystem30

Nucleocapsid mutations in SARS-CoV-2 augment replication and pathogenesis

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