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
-
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
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General Information
General Information on EC 3.5.4.38 - single-stranded DNA cytosine deaminase
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malfunction
metabolism
physiological function
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
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
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