AID/APOBEC deaminases and cancer
暂无分享,去创建一个
Michael Huemer | Richard Greil | R. Greil | S. Rebhandl | M. Huemer | R. Geisberger | Stefan Rebhandl | Roland Geisberger | Stefan Rebhandl
[1] Reuben S Harris,et al. Immunity through DNA deamination. , 2003, Trends in biochemical sciences.
[2] Alexandre Orthwein,et al. Optimal functional levels of activation‐induced deaminase specifically require the Hsp40 DnaJa1 , 2012, The EMBO journal.
[3] M. Kotler,et al. APOBEC3 cytidine deaminases in double-strand DNA break repair and cancer promotion. , 2013, Cancer research.
[4] D. Barnes,et al. Immunoglobulin Isotype Switching Is Inhibited and Somatic Hypermutation Perturbed in UNG-Deficient Mice , 2002, Current Biology.
[5] Reuben S Harris,et al. Comparison of the differential context-dependence of DNA deamination by APOBEC enzymes: correlation with mutation spectra in vivo. , 2004, Journal of molecular biology.
[6] T. Honjo,et al. Specific Expression of Activation-induced Cytidine Deaminase (AID), a Novel Member of the RNA-editing Deaminase Family in Germinal Center B Cells* , 1999, The Journal of Biological Chemistry.
[7] B. Cullen,et al. A second human antiretroviral factor, APOBEC3F, is suppressed by the HIV‐1 and HIV‐2 Vif proteins , 2004, The EMBO journal.
[8] T. Honjo,et al. Class Switch Recombination and Hypermutation Require Activation-Induced Cytidine Deaminase (AID), a Potential RNA Editing Enzyme , 2000, Cell.
[9] Steven A. Roberts,et al. An APOBEC cytidine deaminase mutagenesis pattern is widespread in human cancers , 2013, Nature Genetics.
[10] T. Honjo,et al. De novo protein synthesis is required for the activation-induced cytidine deaminase function in class-switch recombination , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[11] Nicholas O. Davidson,et al. An AU-Rich Sequence Element (UUUN[A/U]U) Downstream of the Edited C in Apolipoprotein B mRNA Is a High-Affinity Binding Site for Apobec-1: Binding of Apobec-1 to This Motif in the 3′ Untranslated Region of c-myc Increases mRNA Stability , 2000, Molecular and Cellular Biology.
[12] M. Taniwaki,et al. Isolation, tissue distribution, and chromosomal localization of the human activation-induced cytidine deaminase (AID) gene. , 2000, Genomics.
[13] S. Conticello. The AID/APOBEC family of nucleic acid mutators , 2008, Genome Biology.
[14] J. Chaudhuri,et al. The splicing regulator PTBP2 is an AID interacting protein and promotes binding of AID to switch region DNA , 2010, Nature Immunology.
[15] Takeshi Kurosu,et al. Human APOBEC3F Is Another Host Factor That Blocks Human Immunodeficiency Virus Type 1 Replication , 2004, Journal of Virology.
[16] Vasco M. Barreto,et al. Regulation of hypermutation by activation-induced cytidine deaminase phosphorylation. , 2006, Proceedings of the National Academy of Sciences of the United States of America.
[17] Reuben S Harris,et al. RNA editing enzyme APOBEC1 and some of its homologs can act as DNA mutators. , 2002, Molecular cell.
[18] Reuben S Harris,et al. The APOBEC3 family of retroelement restriction factors. , 2013, Current topics in microbiology and immunology.
[19] H. Sasaki,et al. APOBEC3B gene overexpression in non-small-cell lung cancer , 2014, Biomedical reports.
[20] Reuben S. Harris,et al. Retroviral restriction by APOBEC proteins , 2004, Nature Reviews Immunology.
[21] D. Boffelli,et al. Activation-induced cytidine deaminase (AID) is necessary for the epithelial–mesenchymal transition in mammary epithelial cells , 2013, Proceedings of the National Academy of Sciences.
[22] F. Alt,et al. The AID antibody diversification enzyme is regulated by protein kinase A phosphorylation , 2005, Nature.
[23] H. Sugimura,et al. Aberrant Expression and Mutation-Inducing Activity of AID in Human Lung Cancer , 2011, Annals of Surgical Oncology.
[24] L. Pasqualucci,et al. AID is required for germinal center–derived lymphomagenesis , 2008, Nature Genetics.
[25] D. Jelinek,et al. Alternative splicing regulates activation-induced cytidine deaminase (AID): implications for suppression of AID mutagenic activity in normal and malignant B cells. , 2008, Blood.
[26] H. Ohno,et al. Activation-induced cytidine deaminase expression in follicular lymphoma: association between AID expression and ongoing mutation in FL , 2004, Leukemia.
[27] M. Neuberger,et al. Deficiency in APOBEC2 Leads to a Shift in Muscle Fiber Type, Diminished Body Mass, and Myopathy , 2009, The Journal of Biological Chemistry.
[28] Vasco M. Barreto,et al. Activation-Induced Cytidine Deaminase Targets DNA at Sites of RNA Polymerase II Stalling by Interaction with Spt5 , 2010, Cell.
[29] S. Mori,et al. In Vivo and In Vitro Studies Suggest a Possible Involvement of HPV Infection in the Early Stage of Breast Carcinogenesis via APOBEC3B Induction , 2014, PloS one.
[30] N. Kakazu,et al. Constitutive Expression of AID Leads to Tumorigenesis , 2003, The Journal of experimental medicine.
[31] S. Henderson,et al. APOBEC-mediated cytosine deamination links PIK3CA helical domain mutations to human papillomavirus-driven tumor development. , 2014, Cell reports.
[32] N. Navaratnam,et al. RNA editing: cytidine to uridine conversion in apolipoprotein B mRNA. , 2000, Biochimica et biophysica acta.
[33] F. Alt,et al. Induction of Activation-induced Cytidine Deaminase Gene Expression by Il-4 and Cd40 Ligation Is Dependent on Stat6 and Nfkb , 2022 .
[34] P. Casali,et al. Immunoglobulin class-switch DNA recombination: induction, targeting and beyond , 2012, Nature Reviews Immunology.
[35] M. Emerman,et al. Polymorphism in Human APOBEC3H Affects a Phenotype Dominant for Subcellular Localization and Antiviral Activity , 2011, Journal of Virology.
[36] S. Pauklin,et al. Estrogen directly activates AID transcription and function , 2009, The Journal of experimental medicine.
[37] K. Kinoshita,et al. Up-regulation of activation-induced cytidine deaminase causes genetic aberrations at the CDKN2b-CDKN2a in gastric cancer. , 2010, Gastroenterology.
[38] R. Rabadán,et al. Noncoding RNA transcription targets AID to divergently transcribed loci in B cells , 2014, Nature.
[39] M. Neuberger,et al. MDM2 can interact with the C-terminus of AID but it is inessential for antibody diversification in DT40 B cells. , 2006, Molecular immunology.
[40] Ralf Küppers,et al. Mechanisms of B-cell lymphoma pathogenesis , 2005, Nature Reviews Cancer.
[41] R. Bende,et al. Activation-Induced Cytidine Deaminase Splice Variants Are Defective Because of the Lack of Structural Support for the Catalytic Site , 2010, The Journal of Immunology.
[42] N A Kolchanov,et al. Somatic hypermutagenesis in immunoglobulin genes. II. Influence of neighbouring base sequences on mutagenesis. , 1992, Biochimica et biophysica acta.
[43] Michel C. Nussenzweig,et al. Translocation-Capture Sequencing Reveals the Extent and Nature of Chromosomal Rearrangements in B Lymphocytes , 2011, Cell.
[44] S. Ambs,et al. Human endogenous retrovirus K and cancer: Innocent bystander or tumorigenic accomplice? , 2014, International journal of cancer.
[45] R. Greil,et al. Alternative splice variants of AID are not stoichiometrically present at the protein level in chronic lymphocytic leukemia , 2014, European journal of immunology.
[46] Seok-Rae Park. Activation-induced Cytidine Deaminase in B Cell Immunity and Cancers , 2012, Immune network.
[47] K. Huebner,et al. FHIT loss-induced DNA damage creates optimal APOBEC substrates: Insights into APOBEC-mediated mutagenesis , 2014, Oncotarget.
[48] Yijun Ruan,et al. B Cell Super-Enhancers and Regulatory Clusters Recruit AID Tumorigenic Activity , 2014, Cell.
[49] M. Neuberger,et al. Molecular mechanisms of antibody somatic hypermutation. , 2007, Annual review of biochemistry.
[50] C. Milstein,et al. Passenger transgenes reveal intrinsic specificity of the antibody hypermutation mechanism: clustering, polarity, and specific hot spots. , 1993, Proceedings of the National Academy of Sciences of the United States of America.
[51] Lela Lackey,et al. APOBEC3B and AID have similar nuclear import mechanisms. , 2012, Journal of molecular biology.
[52] Isora V Sernandez,et al. Haploinsufficiency of Activation-Induced Deaminase for Antibody Diversification and Chromosome Translocations both In Vitro and In Vivo , 2008, PloS one.
[53] David T. W. Jones,et al. Signatures of mutational processes in human cancer , 2013, Nature.
[54] K. Kinoshita,et al. Title Up-regulation of activation-induced cytidine deaminase causesgenetic aberrations at the CDKN 2 b-CDKN 2 a in gastric cancer , 2017 .
[55] M. Nussenzweig,et al. AID Is Required for c-myc/IgH Chromosome Translocations In Vivo , 2004, Cell.
[56] L. Ellis,et al. APOBEC3G promotes liver metastasis in an orthotopic mouse model of colorectal cancer and predicts human hepatic metastasis. , 2011, The Journal of clinical investigation.
[57] A. Fischer,et al. Activation-Induced Cytidine Deaminase (AID) Deficiency Causes the Autosomal Recessive Form of the Hyper-IgM Syndrome (HIGM2) , 2000, Cell.
[58] Wei Lu,et al. A common deletion in the APOBEC3 genes and breast cancer risk. , 2013, Journal of the National Cancer Institute.
[59] V. Diehl,et al. Somatic Mutation of the Cd95 Gene in Human B Cells as a Side-Effect of the Germinal Center Reaction , 2000, The Journal of experimental medicine.
[60] W. Brown,et al. Quantitative profiling of the full APOBEC3 mRNA repertoire in lymphocytes and tissues: implications for HIV-1 restriction , 2010, Nucleic acids research.
[61] M. Neuberger,et al. AID mutates E. coli suggesting a DNA deamination mechanism for antibody diversification , 2002, Nature.
[62] Wolf Reik,et al. Mice Deficient in APOBEC2 and APOBEC3 , 2005, Molecular and Cellular Biology.
[63] C. Münk,et al. An ancient history of gene duplications, fusions and losses in the evolution of APOBEC3 mutators in mammals , 2012, BMC Evolutionary Biology.
[64] A. Børresen-Dale,et al. Mutational Processes Molding the Genomes of 21 Breast Cancers , 2012, Cell.
[65] Y. Yokota,et al. The Balance Between Pax5 and Id2 Activities Is the Key to AID Gene Expression , 2003, The Journal of experimental medicine.
[66] V. I. Mayorov,et al. Mutator effects and mutation signatures of editing deaminases produced in bacteria and yeast , 2011, Biochemistry (Moscow).
[67] M. Goodman,et al. Processive AID-catalysed cytosine deamination on single-stranded DNA simulates somatic hypermutation , 2003, Nature.
[68] F. Alt,et al. Class-switch recombination: interplay of transcription, DNA deamination and DNA repair , 2004, Nature Reviews Immunology.
[69] W. Brown,et al. APOBEC3F Properties and Hypermutation Preferences Indicate Activity against HIV-1 In Vivo , 2004, Current Biology.
[70] N. A. Temiz,et al. APOBEC3B is an enzymatic source of mutation in breast cancer , 2013, Nature.
[71] M. Santiago,et al. Immunoglobulin somatic hypermutation by APOBEC3/Rfv3 during retroviral infection , 2014, Proceedings of the National Academy of Sciences.
[72] A. Ferguson-Smith,et al. Epigenetic reprogramming: is deamination key to active DNA demethylation? , 2011, Reproduction.
[73] James E. Bradner,et al. Convergent Transcription at Intragenic Super-Enhancers Targets AID-Initiated Genomic Instability , 2014, Cell.
[74] M. Shimura,et al. All APOBEC3 family proteins differentially inhibit LINE-1 retrotransposition , 2007, Nucleic acids research.
[75] M. Stratton,et al. DNA deaminases induce break-associated mutation showers with implication of APOBEC3B and 3A in breast cancer kataegis , 2013, eLife.
[76] L. Chan,et al. APOBEC-2, a cardiac- and skeletal muscle-specific member of the cytidine deaminase supergene family. , 1999, Biochemical and biophysical research communications.
[77] T. Honjo,et al. Organ‐specific profiles of genetic changes in cancers caused by activation‐induced cytidine deaminase expression , 2008, International journal of cancer.
[78] F. Alt,et al. Replication protein A interacts with AID to promote deamination of somatic hypermutation targets , 2004, Nature.
[79] T. Lindahl. Instability and decay of the primary structure of DNA , 1993, Nature.
[80] M. Stratton,et al. Subclonal phylogenetic structures in cancer revealed by ultra-deep sequencing , 2008, Proceedings of the National Academy of Sciences.
[81] Cynthia J. Sakofsky,et al. Break-induced replication is a source of mutation clusters underlying kataegis. , 2014, Cell reports.
[82] R. Greil,et al. Lysine Residue at Position 22 of the AID Protein Regulates Its Class Switch Activity , 2012, PloS one.
[83] Reiko Shinkura,et al. Activation-induced cytidine deaminase shuttles between nucleus and cytoplasm like apolipoprotein B mRNA editing catalytic polypeptide 1 , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[84] J. Yates,et al. 14-3-3 adaptor proteins recruit AID to 5′-AGCT-3′-rich switch regions for class switch recombination , 2010, Nature Structural &Molecular Biology.
[85] R. Bende,et al. AID splice variants lack deaminase activity. , 2009, Blood.
[86] M. Neuberger,et al. Evolution of the AID/APOBEC family of polynucleotide (deoxy)cytidine deaminases. , 2005, Molecular biology and evolution.
[87] N. Kadowaki,et al. APOBEC3B can impair genomic stability by inducing base substitutions in genomic DNA in human cells , 2012, Scientific Reports.
[88] M. Neuberger,et al. REG-γ associates with and modulates the abundance of nuclear activation-induced deaminase , 2011, The Journal of experimental medicine.
[89] Adam P Butler,et al. Association of a germline copy number polymorphism of APOBEC3A and APOBEC3B with burden of putative APOBEC-dependent mutations in breast cancer , 2014, Nature Genetics.
[90] B. Chait,et al. Amino-Terminal Phosphorylation of Activation-Induced Cytidine Deaminase Suppresses c-myc/IgH Translocation , 2010, Molecular and Cellular Biology.
[91] D. Gordenin,et al. Hypermutability of Damaged Single-Strand DNA Formed at Double-Strand Breaks and Uncapped Telomeres in Yeast Saccharomyces cerevisiae , 2008, PLoS genetics.
[92] E. Koonin,et al. APOBEC4, a New Member of the AID/APOBEC Family of Polynucleotide (Deoxy)Cytidine Deaminases Predicted by Computational Analysis , 2005, Cell cycle.
[93] R. Greil,et al. AID induces intraclonal diversity and genomic damage in CD86+ chronic lymphocytic leukemia cells , 2014, European journal of immunology.
[94] C. Burant,et al. Molecular cloning of an apolipoprotein B messenger RNA editing protein. , 1993, Science.
[95] F. Alt,et al. Transcription-targeted DNA deamination by the AID antibody diversification enzyme , 2003, Nature.
[96] M. Malim,et al. Isolation of a human gene that inhibits HIV-1 infection and is suppressed by the viral Vif protein , 2002, Nature.
[97] HaroldC. Smith,et al. Functions and regulation of the APOBEC family of proteins. , 2012, Seminars in cell & developmental biology.
[98] T. Molina,et al. The expression of 16 genes related to the cell of origin and immune response predicts survival in elderly patients with diffuse large B-cell lymphoma treated with CHOP and rituximab , 2008, Leukemia.
[99] T. Honjo,et al. Expression of activation-induced cytidine deaminase in human hepatocytes via NF-κB signaling , 2007, Oncogene.
[100] M. Goodman,et al. A Biochemical Analysis Linking APOBEC3A to Disparate HIV-1 Restriction and Skin Cancer* , 2013, The Journal of Biological Chemistry.
[101] R. Espinosa,et al. Assignment of the gene encoding the human apolipoprotein B mRNA editing enzyme (APOBEC1) to chromosome 12p13.1. , 1994, Genomics.
[102] Steven A. Roberts,et al. Clustered mutations in yeast and in human cancers can arise from damaged long single-strand DNA regions. , 2012, Molecular cell.
[103] U. Storb,et al. Mutation of BCL-6 gene in normal B cells by the process of somatic hypermutation of Ig genes. , 1998, Science.
[104] Y. Miki,et al. Identification of novel deletion polymorphisms in breast cancer. , 2008, International journal of oncology.
[105] L. Pasqualucci,et al. BCL-6 mutations in normal germinal center B cells: evidence of somatic hypermutation acting outside Ig loci. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[106] M. Pellegrini,et al. Genome-wide erasure of DNA methylation in mouse primordial germ cells is affected by AID deficiency , 2010, Nature.
[107] Michael M. Mwangi,et al. Transcriptome-wide sequencing reveals numerous APOBEC1 mRNA editing targets in transcript 3′ UTRs , 2010, Nature Structural &Molecular Biology.
[108] Jason C. Young,et al. Regulation of activation-induced deaminase stability and antibody gene diversification by Hsp90 , 2010, The Journal of experimental medicine.
[109] Helen M. Blau,et al. Reprogramming towards pluripotency requires AID-dependent DNA demethylation , 2010, Nature.
[110] I. Dunham,et al. An anthropoid-specific locus of orphan C to U RNA-editing enzymes on chromosome 22. , 2002, Genomics.
[111] A. Furano,et al. Repair of naturally occurring mismatches can induce mutations in flanking DNA , 2014, eLife.
[112] Kefei Yu,et al. Cutting Edge: CTNNBL1 Is Dispensable for Ig Class Switch Recombination , 2010, The Journal of Immunology.
[113] R. Greil,et al. APOBEC3 signature mutations in chronic lymphocytic leukemia , 2014, Leukemia.
[114] V. C. Vieira,et al. The Role of Cytidine Deaminases on Innate Immune Responses against Human Viral Infections , 2013, BioMed research international.
[115] J. Weill,et al. Proteasomal degradation restricts the nuclear lifespan of AID , 2008, The Journal of experimental medicine.
[116] J. Morrison,et al. The p27 catalytic subunit of the apolipoprotein B mRNA editing enzyme is a cytidine deaminase. , 1993, The Journal of biological chemistry.
[117] Jason B. Nikas,et al. APOBEC3B upregulation and genomic mutation patterns in serous ovarian carcinoma. , 2013, Cancer research.
[118] Lela Lackey,et al. Subcellular localization of the APOBEC3 proteins during mitosis and implications for genomic DNA deamination , 2013, Cell cycle.
[119] S. Conticello. Creative deaminases, self‐inflicted damage, and genome evolution , 2012, Annals of the New York Academy of Sciences.
[120] M. Neuberger,et al. AID Is Essential for Immunoglobulin V Gene Conversion in a Cultured B Cell Line , 2002, Current Biology.
[121] I. Willner,et al. APOBEC3G enhances lymphoma cell radioresistance by promoting cytidine deaminase-dependent DNA repair. , 2012, Blood.
[122] M. Stenglein,et al. APOBEC3 proteins mediate the clearance of foreign DNA from human cells , 2010, Nature Structural &Molecular Biology.
[123] S. Sommer,et al. Evidence for mutation showers , 2007, Proceedings of the National Academy of Sciences.
[124] Tomas Lindahl,et al. Repair and genetic consequences of endogenous DNA base damage in mammalian cells. , 2004, Annual review of genetics.
[125] Timothy P. L. Smith,et al. The artiodactyl APOBEC3 innate immune repertoire shows evidence for a multi-functional domain organization that existed in the ancestor of placental mammals , 2008, BMC Molecular Biology.
[126] B. Chait,et al. Regulation of class switch recombination and somatic mutation by AID phosphorylation , 2008, The Journal of experimental medicine.
[127] B. Cairns,et al. DNA Demethylation in Zebrafish Involves the Coupling of a Deaminase, a Glycosylase, and Gadd45 , 2008, Cell.
[128] Samuel H. Wilson. The dark side of DNA repair , 2014, eLife.
[129] S. Cory,et al. Cellular myc oncogene is altered by chromosome translocation to an immunoglobulin locus in murine plasmacytomas and is rearranged similarly in human Burkitt lymphomas. , 1983, Proceedings of the National Academy of Sciences of the United States of America.
[130] M. Malim,et al. Cytidine Deamination of Retroviral DNA by Diverse APOBEC Proteins , 2004, Current Biology.
[131] C. Murre,et al. E-proteins directly regulate expression of activation-induced deaminase in mature B cells , 2003, Nature Immunology.
[132] Z. Szallasi,et al. Spatial and temporal diversity in genomic instability processes defines lung cancer evolution , 2014, Science.
[133] Y. Matsumoto,et al. Accumulation of somatic mutations in TP53 in gastric epithelium with Helicobacter pylori infection. , 2014, Gastroenterology.
[134] Anna Malkova,et al. Migrating bubble during break-induced replication drives conservative DNA synthesis , 2013, Nature.
[135] R. Wall,et al. Somatic hypermutation of the B cell receptor genes B29 (Igbeta, CD79b) and mb1 (Igalpha, CD79a). , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[136] I. Rogozin,et al. AID/APOBEC cytosine deaminase induces genome-wide kataegis , 2012, Biology Direct.
[137] M. Neuberger,et al. Interaction between antibody-diversification enzyme AID and spliceosome-associated factor CTNNBL1. , 2008, Molecular cell.
[138] W. Greene,et al. The APOBEC3 cytidine deaminases: an innate defensive network opposing exogenous retroviruses and endogenous retroelements. , 2008, Annual review of immunology.
[139] M. Neuberger,et al. The stability of AID and its function in class-switching are critically sensitive to the identity of its nuclear-export sequence , 2009, Proceedings of the National Academy of Sciences.
[140] D. Schatz,et al. Two levels of protection for the B cell genome during somatic hypermutation , 2008, Nature.
[141] D. Zhu,et al. Analysis of VH genes in follicular and diffuse lymphoma shows ongoing somatic mutation and multiple isotype transcripts in early disease with changes during disease progression. , 1998, Blood.
[142] M. Goodman,et al. GANP-mediated Recruitment of Activation-induced Cytidine Deaminase to Cell Nuclei and to Immunoglobulin Variable Region DNA* , 2010, The Journal of Biological Chemistry.
[143] M. Goodman,et al. Activation-induced cytidine deaminase deaminates deoxycytidine on single-stranded DNA but requires the action of RNase , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[144] Takeshi Azuma,et al. Helicobacter pylori infection triggers aberrant expression of activation-induced cytidine deaminase in gastric epithelium , 2007, Nature Medicine.
[145] S. Mori,et al. In Vivo and In Vitro Studies Suggest a Possible Involvement of HPV Infection in the Early Stage of Breast Carcinogenesis via APOBEC3B Induction , 2014, PloS one.
[146] Peilin Jia,et al. Patterns and processes of somatic mutations in nine major cancers , 2014, BMC Medical Genomics.
[147] M. Svoboda,et al. Activation-induced cytidine deaminase (AID) linking immunity, chronic inflammation, and cancer , 2012, Cancer Immunology, Immunotherapy.