Nucleotide Weight Matrices Reveal Ubiquitous Mutational Footprints of AID/APOBEC Deaminases in Human Cancer Genomes
Published 2019 View Full Article
- Home
- Publications
- Publication Search
- Publication Details
Title
Nucleotide Weight Matrices Reveal Ubiquitous Mutational Footprints of AID/APOBEC Deaminases in Human Cancer Genomes
Authors
Keywords
-
Journal
Cancers
Volume 11, Issue 2, Pages 211
Publisher
MDPI AG
Online
2019-02-13
DOI
10.3390/cancers11020211
References
Ask authors/readers for more resources
Related references
Note: Only part of the references are listed.- Whole genome sequencing analysis for cancer genomics and precision medicine
- (2018) Hidewaki Nakagawa et al. CANCER SCIENCE
- Comprehensive Characterization of Cancer Driver Genes and Mutations
- (2018) Matthew H. Bailey et al. CELL
- DNA polymerase η mutational signatures are found in a variety of different types of cancer
- (2018) Igor B. Rogozin et al. CELL CYCLE
- Comprehensive Characterization of Cancer Driver Genes and Mutations
- (2018) Matthew H. Bailey et al. CELL
- APOBEC mutation drives early-onset squamous cell carcinomas in recessive dystrophic epidermolysis bullosa
- (2018) Raymond J. Cho et al. Science Translational Medicine
- A Tumor-Promoting Phorbol Ester Causes a Large Increase in APOBEC3A Expression and a Moderate Increase in APOBEC3B Expression in a Normal Human Keratinocyte Cell Line without Increasing Genomic Uracils
- (2018) Sachini U. Siriwardena et al. MOLECULAR AND CELLULAR BIOLOGY
- Exploring background mutational processes to decipher cancer genetic heterogeneity
- (2017) Alexander Goncearenco et al. NUCLEIC ACIDS RESEARCH
- Recombination Is Responsible for the Increased Recovery of Drug-Resistant Mutants with Hypermutated Genomes in Resting Yeast Diploids Expressing APOBEC Deaminases
- (2017) Artem G. Lada et al. Frontiers in Genetics
- Mutational Strand Asymmetries in Cancer Genomes Reveal Mechanisms of DNA Damage and Repair
- (2016) Nicholas J. Haradhvala et al. CELL
- Antibody diversification caused by disrupted mismatch repair and promiscuous DNA polymerases
- (2016) Kimberly J. Zanotti et al. DNA REPAIR
- APOBEC-induced mutations in human cancers are strongly enriched on the lagging DNA strand during replication
- (2016) Vladimir B. Seplyarskiy et al. GENOME RESEARCH
- Structural basis for targeted DNA cytosine deamination and mutagenesis by APOBEC3A and APOBEC3B
- (2016) Ke Shi et al. NATURE STRUCTURAL & MOLECULAR BIOLOGY
- Structural basis for targeted DNA cytosine deamination and mutagenesis by APOBEC3A and APOBEC3B
- (2016) Ke Shi et al. NATURE STRUCTURAL & MOLECULAR BIOLOGY
- Activation induced deaminase mutational signature overlaps with CpG methylation sites in follicular lymphoma and other cancers
- (2016) Igor B. Rogozin et al. Scientific Reports
- The Impact of Environmental and Endogenous Damage on Somatic Mutation Load in Human Skin Fibroblasts
- (2016) Natalie Saini et al. PLoS Genetics
- Clusters of Multiple Mutations: Incidence and Molecular Mechanisms
- (2015) Kin Chan et al. Annual Review of Genetics
- The somatic autosomal mutation matrix in cancer genomes
- (2015) Nuri A. Temiz et al. HUMAN GENETICS
- High burden and pervasive positive selection of somatic mutations in normal human skin
- (2015) I. Martincorena et al. SCIENCE
- Disruption of Transcriptional Coactivator Sub1 Leads to Genome-Wide Re-distribution of Clustered Mutations Induced by APOBEC in Active Yeast Genes
- (2015) Artem G. Lada et al. PLoS Genetics
- Mutational signatures: the patterns of somatic mutations hidden in cancer genomes
- (2014) Ludmil B Alexandrov et al. CURRENT OPINION IN GENETICS & DEVELOPMENT
- Association of a germline copy number polymorphism of APOBEC3A and APOBEC3B with burden of putative APOBEC-dependent mutations in breast cancer
- (2014) Serena Nik-Zainal et al. NATURE GENETICS
- COSMIC: exploring the world's knowledge of somatic mutations in human cancer
- (2014) Simon A. Forbes et al. NUCLEIC ACIDS RESEARCH
- AID and APOBEC deaminases: balancing DNA damage in epigenetics and immunity
- (2014) Don-Marc Franchini et al. Epigenomics
- Active RNAP pre-initiation sites are highly mutated by cytidine deaminases in yeast, with AID targeting small RNA genes
- (2014) Benjamin JM Taylor et al. eLife
- Origins and functional consequences of somatic mitochondrial DNA mutations in human cancer
- (2014) Young Seok Ju et al. eLife
- A Biochemical Analysis Linking APOBEC3A to Disparate HIV-1 Restriction and Skin Cancer
- (2013) Phuong Pham et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- APOBEC3B is an enzymatic source of mutation in breast cancer
- (2013) Michael B. Burns et al. NATURE
- Signatures of mutational processes in human cancer
- (2013) Ludmil B. Alexandrov et al. NATURE
- APOBEC3B mutagenesis in cancer
- (2013) Kawai J Kuong et al. NATURE GENETICS
- Evidence for APOBEC3B mutagenesis in multiple human cancers
- (2013) Michael B Burns et al. NATURE GENETICS
- An APOBEC cytidine deaminase mutagenesis pattern is widespread in human cancers
- (2013) Steven A Roberts et al. NATURE GENETICS
- The Cancer Genome Atlas Pan-Cancer analysis project
- (2013) John N Weinstein et al. NATURE GENETICS
- Signatures of mutational processes in cancer—a big step closer
- (2013) Lisa Hutchinson Nature Reviews Clinical Oncology
- Deciphering Signatures of Mutational Processes Operative in Human Cancer
- (2013) Ludmil B. Alexandrov et al. Cell Reports
- DNA deaminases induce break-associated mutation showers with implication of APOBEC3B and 3A in breast cancer kataegis
- (2013) Benjamin JM Taylor et al. eLife
- 5-Methylcytosine DNA Demethylation: More Than Losing a Methyl Group
- (2012) Don-Marc Franchini et al. Annual Review of Genetics
- Mutator effects and mutation signatures of editing deaminases produced in bacteria and yeast
- (2011) A. G. Lada et al. BIOCHEMISTRY-MOSCOW
- APOBEC3A can activate the DNA damage response and cause cell-cycle arrest
- (2011) Sébastien Landry et al. EMBO REPORTS
Discover Peeref hubs
Discuss science. Find collaborators. Network.
Join a conversationPublish scientific posters with Peeref
Peeref publishes scientific posters from all research disciplines. Our Diamond Open Access policy means free access to content and no publication fees for authors.
Learn More