APOBEC3B-UPDSeq. Escherichia coli

NIAID Data Ecosystem2026-05-01 收录

肿瘤基因组突变机制

APOBEC酶底物特异性

数据链接：

https://www.ncbi.nlm.nih.gov/bioproject/PRJNA1005650 数据链接链接失效反馈

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资源简介：

Distinguishing preferences of human APOBEC3A and APOBEC3B for cytosines in hairpin loops, and reflection of these preferences in APOBEC-signature cancer genome mutations.

创建时间：

2023-08-15

UV-induced DNA lesion mapping in retinoblastoma 1 (RB1) knock out cells. UV-induced DNA lesion mapping in retinoblastoma 1 (RB1) knock out cells

UV诱导DNA损伤

肿瘤基因组突变机制

In this study, we generated a human genome-wide map of DNA lesions induced by ultraviolet (UV) radiation in retinoblastoma knockout (RB1 KO) cells. Interestingly, we observed increased carcinogen susc

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Elevated pyrimidine dimer formation at distinct genomic bases underlie promoter mutation hotspots in UV-exposed cancers

肿瘤基因组突变机制

UV诱导DNA损伤

Sequencing of whole cancer genomes has revealed an abundance of recurrent mutations in gene-regulatorypromoter regions, in particular in melanoma where strong mutation hotspots areobserved adjacent to

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DNA replication initiation shapes the mutational landscape and expression of the human genome (ATAC-Seq). DNA replication initiation shapes the mutational landscape and expression of the human genome (ATAC-Seq)

肿瘤基因组突变机制

DNA复制起始位点

The interplay between active biological processes and DNA repair is central to mutagenesis. We found that the ubiquitous process of replication initiation is mutagenic, leaving a specific mutational f

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The burden of post-translational modification (PTM) – disrupting mutations in the tumor matrisome

肿瘤基因组突变机制

蛋白翻译后修饰

A Pan-cancer analysis of the post-translational modification (PTM) – disrupting mutations in the tumor matrisome

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DNA replication initiation shapes the mutational landscape and expression of the human genome (RNA-Seq)

肿瘤基因组突变机制

基因表达调控

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