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5-methylcytosine in single-stranded DNA + H2O
?
the enzyme exhibits low activity toward 5-methylcytosine n single-stranded DNA
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cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
additional information
?
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cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
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-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
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-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
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-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
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-
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
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-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
activation-induced cytidine deaminase (AID) produces DNA breaks in immunoglobulin genes during antibody diversification. Double-stranded breaks in the switch region mediate class switch recombination, and contribute to gene conversion and somatic hypermutation in the variable regions. Among potential highly transcribed genes in mouse hybridoma cells, the immunoglobulin heavy and light chain genes are important AID targets, with the immunoglobulin mu switch region being preferred compared to other genomic sites
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
activation-induced deaminase is the initiator for somatic hypermutation (SHM) and class switch recombination (CSR). The enzyme targets the highly repetitive switch regions of the immunoglobulin heavy chain locus to induce DNA double-strand breaks (DSBs), which can be rejoined, leading to switch of constant regions of antibody. When targeting to variable region exons of IgH and IgL loci, the enzyme predominantly induces point mutations, termed SHM, resulting in increased affinity of antibody for antigen. While somatic hypermutation and class switch recombination (CSR) enhance antibody diversity, activation-induced deaminase initiated double-strand breaks and mutations may predispose B cells to carcinogenesis
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
AID mediates hypermutation by deaminating single stranded DNA. In vivo, single stranded DNA may arise transiently during transcription
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme can act on transcribing DNA. It is required for the maturation of antibodies in higher vertebrates, where it promotes somatic hypermutation
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme deaminates cytidine residues in the DNA of the variable and the switch regions of the immunoglobulin locus. The resulting uracil induces error-prone DNA synthesis in the case of hypermutation or DNA breaks that activate nonhomologous recombination in the case of class-switch recombination
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme deaminates DNA at transcribed Ig genes. Expressed immunoglobulin genes undergo alterations in sequence and genomic structure in order to optimize antibody function. A single B cell-specific factor, activation-induced deaminase (AID), initiates these changes by deamination of cytosine to uracil. At the Ig loci of B-cells, AID-initiated damage is processed to produce three distinct outcomes: somatic hypermutation, class switch recombination and gene conversion
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme initiates antibody diversification processes by deaminating immunoglobulin sequences
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
activation-induced cytidine deaminase initiates secondary antibody diversification processes by deaminating cytidines on single-stranded DNA. AID preferentially deaminates cytidines preceded by W(A/T)R(A/G) dinucleotides, a sequence specificity that is evolutionarily conserved from bony fish to humans. AID preferentially deaminates bubble substrates of five to seven nucleotides rather than larger bubbles and preferentially binds to bubble-type rather than to single-stranded DNA substrates, suggesting that the natural targets of AID are either transcription bubbles or stem-loop structures. AID displays high affinity for single-stranded DNA. All substrates used in activity assays contain a single cytidine within the bubble and differ in the dinucleotide immediately upstream of the target cytidine constituting either WRC motifs (hot spots) or non-WRC motifs (cold spots)
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
among potential highly transcribed genes in mouse hybridoma cells, the immunoglobulin heavy and light chain genes are important targets, with the immunoglobulin mu switch region being preferred compared to other genomic sites
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
exclusively catalyses deamination of cytidine in single-stranded DNA. It shows minimal activity on stem-loop structures and preferentially deaminates five-nucleotide bubbles. The optimal target consists of a single-stranded NWRCN motif (W = A or T, R = A or G). WRC preference involves the recognition of a purine in the R position and that the carbonyl or amino side chains of guanosine negatively influence specificity at the W position
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?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
no detectable activity on double-stranded DNA. The enzyme catalyzes deoxycytidine to deoxyuridine deamination activity on double-stranded DNA substrates containing a small transcription-like single-stranded DNA bubble. Enzyme activity depends on sequence context
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme deaminates cytidine residues in the DNA of the variable and the switch regions of the immunoglobulin locus. The resulting uracil induces error-prone DNA synthesis in the case of hypermutation or DNA breaks that activate nonhomologous recombination in the case of class-switch recombination. The enzyme deaminates single-stranded but not double-stranded substrates unless it is in a complex with replication protein A (RPA) and the substrate is actively undergoing transcription
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cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme preferentially deaminates cytosine to uracil in single-stranded and not double-stranded DNA the enzyme deaminates DNA at transcribed Ig genes
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the purified, tetrameric enzyme can deaminate cytidine residues in single-stranded DNA, but not in RNA. It deaminates only single-stranded DNA. Neither cytidine nor CTP (or dCTP) are good substrates for the enzyme in vitro
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
conformational equilibrium of the APOBEC3B active site loops, skewed toward being closed, controls enzymatic activity by regulating binding to ssDNA substrates
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the APOBEC3 enzymes are a double-edged sword that can catalyze deamination of cytosine in genomic DNA, which results in potential genomic instability due to the many mutagenic fates of uracil. The enzymes must be able to efficiently deaminate transiently available single-stranded DNA during reverse transcription, replication, or transcription. Specific biochemical characteristics promote deamination in each situation to increase enzyme efficiency through processivity, rapid enzyme cycling between substrates, or oligomerization state
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the APOBEC3 enzymes are a double-edged sword that can catalyze deamination of cytosine in genomic DNA, which results in potential genomic instability due to the many mutagenic fates of uracil. The enzymes must be able to efficiently deaminate transiently available single-stranded DNA during reverse transcription, replication, or transcription. Specific biochemical characteristics promote deamination in each situation to increase enzyme efficiency through processivity, rapid enzyme cycling between substrates, or oligomerization state in DNA
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme restricts the infectivity of viruses, such as HIV-1, by targeting CCC hotspots scattered through minus DNA strands, reverse-transcribed from genomic RNA
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzymes must access single-stranded DNA during the dynamic processes of DNA replication or transcription. The ability of an APOBEC3 to cycle between DNA substrates determines whether it is able to efficiently deaminate single-stranded DNA produced by replication and single-stranded DNA bound by replication protein A. APOBEC3 deaminase activity during transcription has a size limitation that inhibits APOBEC3B tetramers
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cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
deamination activity of methylated cytosine is demonstrated APOBEC3B
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cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
high deaminase activities on cytosine and methylated cytosine with relatively high selectivity for methylated cytosine
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?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
relatively low deaminase activity and selectivity for methylated cytosine
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cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
RNA binding is integral to APOBEC3H function. RNA-mediated dimerization alters the interactions of the enzyme with ssDNA and other RNA molecules
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?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme preferentially converts cytidine to uridine at the third position of triplet cytosine (CCC) hotspots. The phosphate backbone is required for C-terminal domain of the enzyme to slide along the DNA strand and to exert the 3'->5' polarity. The higher the salt cncentration, the less prominent is the 3'->5' polarity
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cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
activation-induced cytidine deaminase (AID) initiates Ig class switch recombination and somatic hypermutation by producing U:G mismatches in DNA. These mismatches also have the potential to induce DNA damage including double-stranded breaks and chromosome translocations
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
activation-induced cytidine deaminase (AID) initiates immunoglobulin class switch DNA recombination (CSR) and somatic hypermutation deaminating deoxycytidines in switch and V(D)J region DNA, respectively, to generate deoxyuracils. Processing of deoxyuracils by uracil DNA glycosylase yields abasic sites, which are excised by apurinic/apyrimidinic endonucleases, eventually generating double strand DNA breaks, the obligatory intermediates of class switch DNA recombination
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?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
activation-induced cytidine deaminase (AID) is a mutator enzyme that initiates somatic mutation and class switch recombination in B lymphocytes by introducing uracil:guanine mismatches into DNA. Repair pathways process these mismatches to produce point mutations in the Ig variable region or double-stranded DNA breaks in the switch region DNA. The enzyme can also produce off-target DNA damage, including mutations in oncogenes
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
activation-induced deaminase is the initiator for somatic hypermutation (SHM) and class switch recombination (CSR). The enzyme targets the highly repetitive switch regions of the immunoglobulin heavy chain locus to induce DNA double-strand breaks (DSBs), which can be rejoined, leading to switch of constant regions of antibody. When targeting to variable region exons of IgH and IgL loci, the enzyme predominantly induces point mutations, termed SHM, resulting in increased affinity of antibody for antigen. While somatic hypermutation and class switch recombination (CSR) enhance antibody diversity, AID initiated double-strand breaks and mutations may predispose B cells to carcinogenesis
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
in response to antigens, B cells undergo two types of genomic alterations to increase antibody diversity. Affinity for antigen can be increased by introduction of point mutations into immunoglobulin heavy (IgH) and immunoglobulin light (IgL) variable regions by somatic hypermutation. Antibody effector functions can be altered by changing the expressed IgH constant region exons through IgH class switch recombination (CSR). Somatic hypermutation and CSR both require the B-cell-specific activation-induced cytidine deaminase protein (AID), which initiates these reactions through its single-stranded DNA-specific cytidine deaminase activity
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme induces reproducible DNA breaks at many non-Ig loci in activated B cells
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme initiates class switch recombination and somatic hypermutation of immunoglobulin genes in B lymphocytes. Activation-induced cytidine deaminase also produces off-target DNA damage, including mutations in oncogenes and double-stranded breaks that can serve as substrates for oncogenic chromosomal translocations
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme initiates Ig heavy chain (IgH) class switch recombination and Ig somatic hypermutation (SHM) by deaminating cytidines within, respectively, IgH switch regions and Ig variable region (V) exons
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?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme does neither catalyzes cytidine to uridine editing of apoB mRNA nor binds to AU-rich RNA targets
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?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
unlike AID-induced double-strand DNA breaks in immunoglobulin genes, genome-wide activation-induced cytidine deaminase-dependent double-strand DNA breaks are not restricted to transcribed regions and frequently occur within repeated sequence elements, including CA repeats, non-CA tandem repeats, and short interspersed element
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?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
-
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
activation-induced deaminase (AID) is involved in processes leading to antibody diversification: somatic hypermutation, gene conversion, and class-switch recombination
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-
?
additional information
?
-
enzyme is able to deaminate 5-methylcytosine in DNA
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?
additional information
?
-
activation-induced cytidine deaminase is function in Pleurodeles waltl. The lack of class switch recombination activity in Pleurodeles waltl is therefore not due to a defect in expression or function of activation-induced cytidine deaminase
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?
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
additional information
?
-
activation-induced cytidine deaminase is function in Pleurodeles waltl. The lack of class switch recombination activity in Pleurodeles waltl is therefore not due to a defect in expression or function of activation-induced cytidine deaminase
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-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
-
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
-
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
-
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
activation-induced cytidine deaminase (AID) produces DNA breaks in immunoglobulin genes during antibody diversification. Double-stranded breaks in the switch region mediate class switch recombination, and contribute to gene conversion and somatic hypermutation in the variable regions. Among potential highly transcribed genes in mouse hybridoma cells, the immunoglobulin heavy and light chain genes are important AID targets, with the immunoglobulin mu switch region being preferred compared to other genomic sites
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
activation-induced deaminase is the initiator for somatic hypermutation (SHM) and class switch recombination (CSR). The enzyme targets the highly repetitive switch regions of the immunoglobulin heavy chain locus to induce DNA double-strand breaks (DSBs), which can be rejoined, leading to switch of constant regions of antibody. When targeting to variable region exons of IgH and IgL loci, the enzyme predominantly induces point mutations, termed SHM, resulting in increased affinity of antibody for antigen. While somatic hypermutation and class switch recombination (CSR) enhance antibody diversity, activation-induced deaminase initiated double-strand breaks and mutations may predispose B cells to carcinogenesis
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
AID mediates hypermutation by deaminating single stranded DNA. In vivo, single stranded DNA may arise transiently during transcription
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme can act on transcribing DNA. It is required for the maturation of antibodies in higher vertebrates, where it promotes somatic hypermutation
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme deaminates cytidine residues in the DNA of the variable and the switch regions of the immunoglobulin locus. The resulting uracil induces error-prone DNA synthesis in the case of hypermutation or DNA breaks that activate nonhomologous recombination in the case of class-switch recombination
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme deaminates DNA at transcribed Ig genes. Expressed immunoglobulin genes undergo alterations in sequence and genomic structure in order to optimize antibody function. A single B cell-specific factor, activation-induced deaminase (AID), initiates these changes by deamination of cytosine to uracil. At the Ig loci of B-cells, AID-initiated damage is processed to produce three distinct outcomes: somatic hypermutation, class switch recombination and gene conversion
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme initiates antibody diversification processes by deaminating immunoglobulin sequences
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
conformational equilibrium of the APOBEC3B active site loops, skewed toward being closed, controls enzymatic activity by regulating binding to ssDNA substrates
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the APOBEC3 enzymes are a double-edged sword that can catalyze deamination of cytosine in genomic DNA, which results in potential genomic instability due to the many mutagenic fates of uracil. The enzymes must be able to efficiently deaminate transiently available single-stranded DNA during reverse transcription, replication, or transcription. Specific biochemical characteristics promote deamination in each situation to increase enzyme efficiency through processivity, rapid enzyme cycling between substrates, or oligomerization state
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the APOBEC3 enzymes are a double-edged sword that can catalyze deamination of cytosine in genomic DNA, which results in potential genomic instability due to the many mutagenic fates of uracil. The enzymes must be able to efficiently deaminate transiently available single-stranded DNA during reverse transcription, replication, or transcription. Specific biochemical characteristics promote deamination in each situation to increase enzyme efficiency through processivity, rapid enzyme cycling between substrates, or oligomerization state in DNA
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme restricts the infectivity of viruses, such as HIV-1, by targeting CCC hotspots scattered through minus DNA strands, reverse-transcribed from genomic RNA
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzymes must access single-stranded DNA during the dynamic processes of DNA replication or transcription. The ability of an APOBEC3 to cycle between DNA substrates determines whether it is able to efficiently deaminate single-stranded DNA produced by replication and single-stranded DNA bound by replication protein A. APOBEC3 deaminase activity during transcription has a size limitation that inhibits APOBEC3B tetramers
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
activation-induced cytidine deaminase (AID) initiates Ig class switch recombination and somatic hypermutation by producing U:G mismatches in DNA. These mismatches also have the potential to induce DNA damage including double-stranded breaks and chromosome translocations
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
activation-induced cytidine deaminase (AID) initiates immunoglobulin class switch DNA recombination (CSR) and somatic hypermutation deaminating deoxycytidines in switch and V(D)J region DNA, respectively, to generate deoxyuracils. Processing of deoxyuracils by uracil DNA glycosylase yields abasic sites, which are excised by apurinic/apyrimidinic endonucleases, eventually generating double strand DNA breaks, the obligatory intermediates of class switch DNA recombination
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
activation-induced cytidine deaminase (AID) is a mutator enzyme that initiates somatic mutation and class switch recombination in B lymphocytes by introducing uracil:guanine mismatches into DNA. Repair pathways process these mismatches to produce point mutations in the Ig variable region or double-stranded DNA breaks in the switch region DNA. The enzyme can also produce off-target DNA damage, including mutations in oncogenes
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
activation-induced deaminase is the initiator for somatic hypermutation (SHM) and class switch recombination (CSR). The enzyme targets the highly repetitive switch regions of the immunoglobulin heavy chain locus to induce DNA double-strand breaks (DSBs), which can be rejoined, leading to switch of constant regions of antibody. When targeting to variable region exons of IgH and IgL loci, the enzyme predominantly induces point mutations, termed SHM, resulting in increased affinity of antibody for antigen. While somatic hypermutation and class switch recombination (CSR) enhance antibody diversity, AID initiated double-strand breaks and mutations may predispose B cells to carcinogenesis
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
in response to antigens, B cells undergo two types of genomic alterations to increase antibody diversity. Affinity for antigen can be increased by introduction of point mutations into immunoglobulin heavy (IgH) and immunoglobulin light (IgL) variable regions by somatic hypermutation. Antibody effector functions can be altered by changing the expressed IgH constant region exons through IgH class switch recombination (CSR). Somatic hypermutation and CSR both require the B-cell-specific activation-induced cytidine deaminase protein (AID), which initiates these reactions through its single-stranded DNA-specific cytidine deaminase activity
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme induces reproducible DNA breaks at many non-Ig loci in activated B cells
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme initiates class switch recombination and somatic hypermutation of immunoglobulin genes in B lymphocytes. Activation-induced cytidine deaminase also produces off-target DNA damage, including mutations in oncogenes and double-stranded breaks that can serve as substrates for oncogenic chromosomal translocations
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
the enzyme initiates Ig heavy chain (IgH) class switch recombination and Ig somatic hypermutation (SHM) by deaminating cytidines within, respectively, IgH switch regions and Ig variable region (V) exons
-
-
?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
activation-induced deaminase (AID) is involved in processes leading to antibody diversification: somatic hypermutation, gene conversion, and class-switch recombination
-
-
?
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malfunction
deficiency in activation-induced deaminase is responsible for a human immunodeficiency
malfunction
when aberrantly expressed in lung or breast tissue, APOBEC3H can contribute to cancer mutagenesis
metabolism
activation-induced deaminase initiated double-strand breaks and mutations may predispose B cells to carcinogenesis
metabolism
APOBEC3B-catalyzed DNA cytosine deamination causes mutations in cancer
metabolism
the APOBEC3 family has many roles, such as restricting endogenous and exogenous retrovirus replication and retrotransposon insertion events and reducing DNA-induced inflammation
metabolism
the enzyme can contribute to cancer through deamination of cytosine to form promutagenic uracil in genomic DNA
metabolism
the enzyme generates cytidine to deoxyuridine mutations in single-stranded DNA, and is capable of restricting replication of HIV-1 by generating mutations in viral genome
physiological function
activation-induced cytidine deaminase (AID) initiates Ig class switch recombination and somatic hypermutation by producing U:G mismatches in DNA. These mismatches also have the potential to induce DNA damage including double-stranded breaks and chromosome translocations
physiological function
activation-induced cytidine deaminase (AID) initiates immunoglobulin class switch DNA recombination (CSR) and somatic hypermutation deaminating deoxycytidines in switch and V(D)J region DNA,respectively, to generate deoxyuracils. Processing of deoxyuracils by uracil DNA glycosylase yields abasic sites, which are excised by apurinic/apyrimidinic endonucleases, eventually generating double strand DNA breaks, the obligatory intermediates of class switch DNA recombination
physiological function
activation-induced cytidine deaminase (AID) is a mutator enzyme that initiates somatic mutation and class switch recombination in B lymphocytes by introducing uracil:guanine mismatches into DNA. Repair pathways process these mismatches to produce point mutations in the Ig variable region or double-stranded DNA breaks in the switch region DNA. The enzyme can also produce off-target DNA damage, including mutations in oncogenes
physiological function
activation-induced cytidine deaminase (AID) produces DNA breaks in immunoglobulin genes during antibody diversification. Double-stranded breaks (DSB) in the switch region mediate class switch recombination, and contribute to gene conversion and somatic hypermutation in the variable regions
physiological function
activation-induced deaminase (AID) is involved in processes leading to antibody diversification: somatic hypermutation, gene conversion, and class-switch recombination
physiological function
AID mediates hypermutation by deaminating single stranded DNA. In vivo, single stranded DNA may arise transiently during transcription
physiological function
expressed immunoglobulin genes undergo alterations in sequence and genomic structure in order to optimize antibody function. The B cell-specific activation-induced deaminase (AID), initiates these changes by deamination of cytosine to uracil. At the Ig loci of B-cells, AID-initiated damage is processed to produce three distinct outcomes: somatic hypermutation, class switch recombination and gene conversion
physiological function
in response to antigens, B cells undergo two types of genomic alterations to increase antibody diversity. Affinity for antigen can be increased by introduction of point mutations into immunoglobulin heavy (IgH) and immunoglobulin light (IgL) variable regions by somatic hypermutation. Antibody effector functions can be altered by changing the expressed IgH constant region exons through IgH class switch recombination (CSR). Somatic hypermutation and CSR both require the B-cell-specific activation-induced cytidine deaminase protein (AID), which initiates these reactions through its single-stranded DNA-specific cytidine deaminase activity
physiological function
the enzyme induces reproducible DNA breaks at many non-Ig loci in activated B cells
physiological function
the enzyme initiates antibody diversification processes by deaminating immunoglobulin sequences
physiological function
the enzyme initiates class switch recombination and somatic hypermutation of immunoglobulin genes in B lymphocytes. Activation-induced cytidine deaminase also produces off-target DNA damage, including mutations in oncogenes and double-stranded breaks that can serve as substrates for oncogenic chromosomal translocations
physiological function
the enzyme is involved in immunoglobulin affinity maturation, gene conversion and class switch recombination. This protein is therefore a major actor in the creation of the antibody repertoire
physiological function
the enzyme is required for the maturation of antibodies in higher vertebrates, where it promotes somatic hypermutation
physiological function
AICDA-/- induced pluripotent stem cells fail to achieve the naive pluripotent state and remain primed for differentiation because of a failure to suppress fibroblast growth factor FGF/extracellular signal-regulated kinases ERK signaling. The mutant cells display marked genomic hypermethylation, but suppression of FGF/ERK signaling by AICDA is independent of deaminase activity
physiological function
APOBEC3A, a is a C>U RNA-editing enzyme that modifies the monocyte/macrophage transcriptome. Transcripts of hundreds of genes undergo sitespecific C>U RNA editing in macrophages during M1 polarization and in monocytes in response to hypoxia and interferons. Amino acid residues of APOBEC3A that are required for its DNA deamination and anti-retrotransposition activities also affect its RNA deamination activity
physiological function
APOBEC3G causes site-specific C-to-U editing of mRNAs from over 600 genes. The edited cytidines are often flanked by inverted repeats, but are largely distinct from those deaminated by isoform APOBEC3A. Both the N-terminal and C-terminal doman are required for the NA editing function
physiological function
APOBEC3Z1 induces double strand DNA breaks and apoptosis upon expression in HeLa cells
physiological function
both heterogeneous nuclear ribonucleoproteins hnRNP K and L exhibit RNA-dependent interactions with AID and are required for antibody class switch recombination. Depletion of hnRNP K reduces somatic hypermutation, and hnRNP K is required for AID-induced DNA breaks
physiological function
the enzyme has important roles in innate immunity but is also a major endogenous source of mutations in cancer
physiological function
the enzyme inhibits replication of retroelements and HIV-1 in CD4+ T cells
physiological function
the enzyme initiates somatic hypermutation and class-switch recombination by deaminating C -> U during transcription of Ig-variable and Ig-switch region DNA, which is essential to produce high-affinity antibodies
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Larijani, M.;Petrov, A.P.; Kolenchenko, O.; Berru, M.; Krylov, S.N.; Martin, A.
AID associates with single-stranded DNA with high affinity and a long complex half-life in a sequence-independent manner
Mol. Cell. Biol.
27
20-30
2007
Homo sapiens (Q9GZX7)
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Vallur, A.C.; Yabuki, M.; Larson, E.D.; Maizels, N.
AID in antibody perfection
Cell. Mol. Life Sci.
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555-565
2007
Homo sapiens (Q9GZX7)
brenda
Brar, S.S.; Sacho, E.J.; Tessmer, I.; Croteau, D.L.; Erie, D.A.; Diaz, M.
Activation-induced deaminase, AID, is catalytically active as a monomer on single-stranded DNA
DNA Repair
7
77-87
2007
Homo sapiens (Q9GZX7)
brenda
Carpenter, M.A.; Rajagurubandara, E.; Wijesinghe, P.; Bhagwat, A.S.
Determinants of sequence-specificity within human AID and APOBEC3G
DNA Repair
9
579-587
2010
Homo sapiens (Q9GZX7), Homo sapiens
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Lee, S.A.; Parsa, J.Y.; Martin, A.; Baker, M.D.
Activation-induced cytidine deaminase induces DNA break repair events more frequently in the Ig switch region than other sites in the mammalian genome
Eur. J. Immunol.
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2007
Homo sapiens (Q9GZX7)
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Wang, J.H.
The role of activation-induced deaminase in antibody diversification and genomic instability
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Homo sapiens (Q9GZX7), Mus musculus (Q9WVE0)
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Muramatsu, M.; Sankaranand, V.S.; Anant, S.; Sugai, M.; Kinoshita, K.; Davidson, N.O.; Honjo, T.
Specific expression of activation-induced cytidine deaminase (AID), a novel member of the RNA-editing deaminase family in germinal center B cells
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Mus musculus (Q9WVE0), Mus musculus
brenda
Li, G.; Pone, E.J.; Tran, D.C.; Patel, P.J.; Dao, L.; Xu, Z.; Casali, P.
Iron inhibits activation-induced cytidine deaminase enzymatic activity and modulates immunoglobulin class switch DNA recombination
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2012
Mus musculus (Q9WVE0)
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AID mediates hypermutation by deaminating single stranded DNA
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2003
Homo sapiens (Q9GZX7)
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Aoufouchi, S.; Faili, A.; Zober, C.; D'Orlando, O.; Weller, S.; Weill, J.C.; Reynaud, C.A.
Proteasomal degradation restricts the nuclear lifespan of AID
J. Exp. Med.
205
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2008
Homo sapiens (Q9GZX7)
brenda
McBride, K.M.; Gazumyan, A.; Woo, E.M.; Schwickert, T.A.; Chait, B.T.; Nussenzweig, M.C.
Regulation of class switch recombination and somatic mutation by AID phosphorylation
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205
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2008
Mus musculus (Q9WVE0)
brenda
Miyazaki, Y.; Inoue, H.; Kikuchi, K.; Ochiai, K.; Kusama, K.
Activation-induced cytidine deaminase mRNA expression in oral squamous cell carcinoma-derived cell lines is upregulated by inflammatory cytokines
J. Oral Sci.
54
71-75
2012
Homo sapiens (Q9GZX7)
brenda
Larijani, M.; Martin, A.
Single-stranded DNA structure and positional context of the target cytidine determine the enzymatic efficiency of AID
Mol. Cell. Biol.
27
8038-8048
2007
Homo sapiens (Q9GZX7)
brenda
Gazumyan, A.; Timachova, K.; Yuen, G.; Siden, E.; Di Virgilio, M.; Woo, E.M.; Chait, B.T.; San-Martin, B.R.; Nussenzweig, M.C.; McBride, K.M.
Amino-terminal phosphorylation of activation-induced cytidine deaminase suppresses c-myc/IgH translocation
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31
442-449
2011
Mus musculus (Q9WVE0)
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Staszewski, O.; Baker, R.E.; Ucher, A.J.; Martier, R.; Stavnezer, J.; Guikema, J.E.
Activation-induced cytidine deaminase induces reproducible DNA breaks at many non-Ig loci in activated B cells
Mol. Cell.
41
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2011
Mus musculus (Q9WVE0)
brenda
Bascove, M.; Frippiat, J.P.
Molecular characterization of Pleurodeles waltl activation-induced cytidine deaminase
Mol. Immunol.
47
1640-1649
2010
Pleurodeles waltl (D5GRW1)
brenda
Basu, U.; Chaudhuri, J.; Alpert, C.; Dutt, S.; Ranganath, S.; Li, G.; Schrum, J.P.; Manis, J.P.; Alt, F.W.
The AID antibody diversification enzyme is regulated by protein kinase A phosphorylation
Nature
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508-511
2005
Mus musculus (Q9WVE0)
brenda
Sohail, A.; Klapacz, J.; Samaranayake, M.; Ullah, A.; Bhagwat, A.S.
Human activation-induced cytidine deaminase causes transcription-dependent, strand-biased C to U deaminations
Nucleic Acids Res.
31
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2003
Homo sapiens (Q9GZX7)
brenda
Bransteitter, R.; Pham, P.; Scharff, M.D.; Goodman, M.F.
Activation-induced cytidine deaminase deaminates deoxycytidine on single-stranded DNA but requires the action of RNase
Proc. Natl. Acad. Sci. USA
100
4102-4107
2003
Homo sapiens (Q9GZX7)
brenda
Yang, G.; Obiakor, H.; Sinha, R.K.; Newman, B.A.; Hood, B.L.; Conrads, T.P.; Veenstra, T.D.; Mage, R.G.
Activation-induced deaminase cloning, localization, and protein extraction from young VH-mutant rabbit appendix
Proc. Natl. Acad. Sci. USA
102
17083-17088
2005
Oryctolagus cuniculus (Q3BAF8), Oryctolagus cuniculus
brenda
Pasqualucci, L.; Kitaura, Y.; Gu, H.; Dalla-Favera, R.
PKA-mediated phosphorylation regulates the function of activation-induced deaminase (AID) in B cells
Proc. Natl. Acad. Sci. USA
103
395-400
2005
Homo sapiens (Q9GZX7)
brenda
McBride, K.M.; Gazumyan, A.; Woo, E.M.; Barreto, V.M.; Robbiani, D.F.; Chait, B.T.; Nussenzweig, M.C.
Regulation of hypermutation by activation-induced cytidine deaminase phosphorylation
Proc. Natl. Acad. Sci. USA
103
8798-8803
2006
Mus musculus (Q9WVE0)
brenda
Cheng, H.L.; Vuong, B.Q.; Basu, U.; Franklin, A.; Schwer, B.; Astarita, J.; Phan, R.T.; Datta, A.; Manis, J.; Alt, F.W.; Chaudhuri, J.
Integrity of the AID serine-38 phosphorylation site is critical for class switch recombination and somatic hypermutation in mice
Proc. Natl. Acad. Sci. USA
106
2717-2122
2009
Mus musculus (Q9WVE0)
brenda
Meyers, G.; Ng, Y.S.; Bannock, J.M.; Lavoie, A.; Walter, J.E.; Notarangelo, L.D.; Kilic, S.S.; Aksu, G.; Debre, M.; Rieux-Laucat, F.; Conley, M.E.; Cunningham-Rundles, C.; Durandy, A.; Meffre, E.
Activation-induced cytidine deaminase (AID) is required for B-cell tolerance in humans
Proc. Natl. Acad. Sci. USA
108
11554-11559
2011
Homo sapiens
brenda
Kuraoka, M.; Holl, T.M.; Liao, D.; Womble, M.; Cain, D.W.; Reynolds, A.E.; Kelsoe, G.
Activation-induced cytidine deaminase mediates central tolerance in B cells
Proc. Natl. Acad. Sci. USA
108
11560-11565
2011
Mus musculus
brenda
Verma, S.; Goldammer, T.; Aitken, R.
Cloning and expression of activation induced cytidine deaminase from Bos taurus
Vet. Immunol. Immunopathol.
134
151-159
2010
Bos taurus (Q2PT36)
brenda
Bae, S.J.; Park, B.G.; Kim, B.G.; Hahn, J.S.
Multiplex gene disruption by targeted base editing of Yarrowia lipolytica genome using cytidine deaminase combined with the CRISPR/Cas9 system
Biotechnol. J.
2019
e1900238
2019
Petromyzon marinus
brenda
Hou, S.; Silvas, T.V.; Leidner, F.; Nalivaika, E.A.; Matsuo, H.; Kurt Yilmaz, N.; Schiffer, C.A.
Structural analysis of the active site and DNA binding of human cytidine deaminase APOBEC3B
J. Chem. Theory Comput.
15
637-647
2019
Homo sapiens (Q9UH17), Homo sapiens
brenda
Sharma, S.; Patnaik, S.K.; Taggart, R.T.; Kannisto, E.D.; Enriquez, S.M.; Gollnick, P.; Baysal, B.E.
APOBEC3A cytidine deaminase induces RNA editing in monocytes and macrophages
Nat. Commun.
6
6881
2015
Homo sapiens (P31941)
brenda
Hu, W.; Begum, N.A.; Mondal, S.; Stanlie, A.; Honjo, T.
Identification of DNA cleavage- and recombination-specific hnRNP cofactors for activation-induced cytidine deaminase
Proc. Natl. Acad. Sci. USA
112
5791-5796
2015
Homo sapiens (Q9GZX7)
brenda
Marx, A.; Galilee, M.; Alian, A.
Zinc enhancement of cytidine deaminase activity highlights a potential allosteric role of loop-3 in regulating APOBEC3 enzymes
Sci. Rep.
5
18191
2015
Homo sapiens (P31941), Homo sapiens (Q9HC16)
brenda
Sharma, S.; Patnaik, S.K.; Taggart, R.T.; Baysal, B.E.
The double-domain cytidine deaminase APOBEC3G is a cellular site-specific RNA editing enzyme
Sci. Rep.
6
39100
2016
Homo sapiens (Q9HC16)
brenda
Li, X.; Caval, V.; Wain-Hobson, S.; Vartanian, J.P.
Elephant APOBEC3A cytidine deaminase induces massive double-stranded DNA breaks and apoptosis
Sci. Rep.
9
728
2019
Loxodonta africana (A0A4Y5QRZ7)
brenda
Kumar, R.; Evans, T.
Activation-induced cytidine deaminase regulates fibroblast growth factor/extracellular signal-regulated kinases signaling to achieve the naive pluripotent state during reprogramming
Stem Cells
37
1003-1017
2019
Mus musculus (Q9WVE0)
brenda
King, J.J.; Manuel, C.A.; Barrett, C.V.; Raber, S.; Lucas, H.; Sutter, P.; Larijani, M.
Catalytic pocket inaccessibility of activation-induced cytidine deaminase is a safeguard against excessive mutagenic activity
Structure
23
615-627
2015
Homo sapiens, Homo sapiens (P31941)
brenda
Adolph, M.B.; Love, R.P.; Chelico, L.
Biochemical basis of APOBEC3 deoxycytidine deaminase activity on diverse DNA substrates
ACS Infect. Dis.
4
224-238
2018
Homo sapiens (P31941), Homo sapiens (Q6NTF7), Homo sapiens (Q8IUX4), Homo sapiens (Q96AK3), Homo sapiens (Q9HC16), Homo sapiens (Q9NRW3), Homo sapiens (Q9UH17)
brenda
Pham, P.; Afif, S.A.; Shimoda, M.; Maeda, K.; Sakaguchi, N.; Pedersen, L.C.; Goodman, M.F.
Structural analysis of the activation-induced deoxycytidine deaminase required in immunoglobulin diversification
DNA Repair
43
48-56
2016
Escherichia coli O157:H7 (P0AEY0)
brenda
Shi, K.; Carpenter, M.A.; Kurahashi, K.; Harris, R.S.; Aihara, H.
Crystal structure of the DNA deaminase APOBEC3B catalytic domain
J. Biol. Chem.
290
28120-28130
2015
Homo sapiens (Q9UH17)
brenda
Ito, F.; Fu, Y.; Kao, S.A.; Yang, H.; Chen, X.S.
Family-wide comparative analysis of cytidine and methylcytidine deamination by eleven human APOBEC proteins
J. Mol. Biol.
429
1787-1799
2017
Homo sapiens (P31941), Homo sapiens (Q6NTF7), Homo sapiens (Q8IUX4), Homo sapiens (Q96AK3), Homo sapiens (Q9HC16), Homo sapiens (Q9NRW3), Homo sapiens (Q9UH17), Homo sapiens
brenda
Feng, Y.; Wong, L.; Morse, M.; Rouzina, I.; Williams, M.C.; Chelico, L.
RNA-mediated dimerization of the human deoxycytidine deaminase APOBEC3H influences enzyme activity and interaction with nucleic acids
J. Mol. Biol.
430
4891-4907
2018
Homo sapiens (Q6NTF7), Homo sapiens
brenda
Fang, Y.; Xiao, X.; Li, S.X.; Wolfe, A.; Chen, X.S.
Molecular interactions of a DNA modifying enzyme APOBEC3F catalytic domain with a single-stranded DNA
J. Mol. Biol.
430
87-101
2018
Homo sapiens (Q8IUX4)
brenda
Maiti, A.; Myint, W.; Kanai, T.; Delviks-Frankenberry, K.; Sierra Rodriguez, C.; Pathak, V.K.; Schiffer, C.A.; Matsuo, H.
Crystal structure of the catalytic domain of HIV-1 restriction factor APOBEC3G in complex with sDNA
Nat. Commun.
9
2460
2018
Homo sapiens (Q9HC16)
brenda
Adolph, M.B.; Love, R.P.; Feng, Y.; Chelico, L.
Enzyme cycling contributes to efficient induction of genome mutagenesis by the cytidine deaminase APOBEC3B
Nucleic Acids Res.
45
11925-11940
2017
Homo sapiens (Q9UH17)
brenda
Wang, Y.; Wu, S.; Zheng, S.; Wang, S.; Wali, A.; Ezhilarasan, R.; Sulman, E.P.; Koul, D.; Alfred Yung, W.K.
APOBEC3G acts as a therapeutic target in mesenchymal gliomas by sensitizing cells to radiation-induced cell death
Oncotarget
8
54285-54296
2017
Homo sapiens (Q9HC16)
brenda
Kamba, K.; Nagata, T.; Katahira, M.
Catalytic analysis of APOBEC3G involving real-time NMR spectroscopy reveals nucleic acid determinants for deamination
PLoS ONE
10
e0124142
2015
Homo sapiens (Q9HC16)
brenda
Shi, K.; Demir, O.e.; Carpenter, M.A.; Wagner, J.; Kurahashi, K.; Harris, R.S.; Amaro, R.E.; Aihara, H.
Conformational switch regulates the DNA cytosine deaminase activity of human APOBEC3B
Sci. Rep.
7
17415
2017
Homo sapiens (Q9UH17), Homo sapiens
brenda