3.5.4.38: single-stranded DNA cytosine deaminase
This is an abbreviated version!
For detailed information about single-stranded DNA cytosine deaminase, go to the full flat file.
Word Map on EC 3.5.4.38
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3.5.4.38
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apobec3s
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deamination
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hypermutation
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deaminases
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immunoglobulin
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uracil
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viruses
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apolipoprotein
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retroviruses
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diversification
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ige
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virion
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polypeptide-like
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retroviral
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mrna-editing
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retrotransposons
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antiretroviral
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retroelements
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vif-deficient
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anti-hiv-1
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retrotransposition
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class-switching
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glycosylase
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lentiviruses
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uracil-dna
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line-1
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proviral
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vif-mediated
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aid-dependent
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cccdna
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aid-induced
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abasic
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c-to-u
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encapsidation
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translesion
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r-loops
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sivmac
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molecular biology
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samhd1
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medicine
- 3.5.4.38
- apobec3s
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deamination
-
hypermutation
- deaminases
- immunoglobulin
- uracil
- viruses
-
apolipoprotein
- retroviruses
-
diversification
- ige
- virion
-
polypeptide-like
-
retroviral
-
mrna-editing
-
retrotransposons
-
antiretroviral
-
retroelements
-
vif-deficient
-
anti-hiv-1
-
retrotransposition
-
class-switching
- glycosylase
- lentiviruses
-
uracil-dna
-
line-1
-
proviral
-
vif-mediated
-
aid-dependent
-
cccdna
-
aid-induced
-
abasic
-
c-to-u
-
encapsidation
-
translesion
-
r-loops
-
sivmac
- molecular biology
- samhd1
- medicine
Reaction
Synonyms
A3F, activation-induced cytidine deaminase, activation-induced deaminase, AICDA, AID, APOBEC3A, APOBEC3B, APOBEC3C, APOBEC3D, APOBEC3F, APOBEC3G, APOBEC3H, APOBEC3Z1, CDA1, single-stranded (ss)DNA deoxycytidine deaminase, ssDNA cytidine deaminase
ECTree
3.5.4.38 single-stranded DNA cytosine deaminaseAdvanced search results
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results (Natural Substrates Products
Natural Substrates Products on EC 3.5.4.38 - single-stranded DNA cytosine deaminase
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NATURAL SUBSTRATE 
NATURAL PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
REVERSIBILITY
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
additional information
?
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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
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?
cytosine in single-stranded DNA + H2O
uracil in single-stranded DNA + NH3
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-
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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
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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, activation-induced deaminase initiated double-strand breaks and mutations may predispose B cells to carcinogenesis
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?
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
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?
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
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
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
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-
?
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
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?
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
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?
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
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?
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
activation-induced deaminase (AID) is involved in processes leading to antibody diversification: somatic hypermutation, gene conversion, and class-switch recombination
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-
?
