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Synonyms
apobec3b, apobec3a, apobec3f, activation-induced deaminase, apobec3h, apobec3c, apobec3d, single-stranded dna cytosine deaminase, apobec3z1, ssdna 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
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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
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 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
-
-
?
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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
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 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
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
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phosphoprotein
515% of the enzyme expressed in activated B cells is phosphorylated at Ser38. The modified form contributes disproportionately to hypermutation. This form of activation-induced cytidine deaminase is enriched in the chromatin fraction in activated B cells
phosphoprotein
activation-induced cytidine deaminase that is phosphorylated on serine residue 38 interacts with replication protein A, a ssDNA binding protein, to promote deamination of transcribed double-stranded DNA in vitro. The Ser38 phosphorylation site is required for normal class switch recombination and Ig somatic hypermutation in mice
phosphoprotein
in addition to Ser38, the enzyme is also phosphorylated at position Thr140. Mutation of either Ser38 or Thr140 to Ala does not impact catalytic activity, but interfers with class switching and somatic hypermutation in vivo. Ser38 is equally important for both processes, Thr140 phosphorylation preferentially affects somatic mutation
phosphoprotein
phosphorylation at serine 38 and threonine 140 increases activity. Activation-induced cytidine deaminase activity and its oncogenic potential can be downregulated by phosphorylation of Ser3. This process is controlled by serine/threonine protein phosphatase 2A
phosphoprotein
protein kinase A phosphorylates the Ser38. This phosphorylation event activates the enzyme to enable interaction with replication protein A, thereby augmenting the ability of activation-induced cytidine deaminase to effect class switch recombination in vivo
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S3A
purified recombinant mutant enzyme S3A and wild-type have similar deamination activities on an ssDNA substrate in vitro. AID-/- B cells expressing AIDS3A show a consistently higher percentage of class-switched IgG1-expressing B cells than control enzyme. Mutating S3 to A does not alter catalysis but does result in increased AID activity in class switch recombination
S3D
AID-/- B cells expressing AID-S3D show a consistently higher percentage of class-switched IgG1-expressing B cells than control enzyme. Mutating S3 to A does not alter catalysis but does result in increased AID activity in class switch recombination
T140A
mutation does not impact catalytic activity, but interfers with class switching and somatic hypermutation in vivo
additional information
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generation of several enzyme-deficient Aicda-/- mice
S38A
mutant form of activation-induced cytidine deaminase that retains similar catalytic activity on ssDNA as wild-type enzyme. The AIDS38A mutant protein is significantly compromised in its ability to mediate somatic hypermutation SHM. B cells homozygous for the AIDS38A mutation show substantially impaired class switch recombination and Ig somatic hypermutation, correlating with inability of AIDS38A to interact with endogenous replication protein A. Mice haploinsufficient for AIDS38A have more severely impaired class switch recombination when compared with mice haploinsufficient for AIDWT, with class switch recombination levels reduced to nearly background levels. These results unequivocally demonstrate that integrity of the AID S38 phosphorylation site is required for normal class switch recombination and Ig somatic hypermutation in mice and support a role for AID phosphorylation at S38 and replication protein A interaction in regulating class switch recombination and Ig somatic hypermutation
S38A
mutation does not impact catalytic activity, but interfers with class switching and somatic hypermutation in vivo
S38A
the kinetics of single-stranded DNA deaminase activity for wild-type and S38A mutant enzyme are comparable
S38A
the mutant enzyme shows dimished somatic hypermutation activity on artificial and physiological DNA targets
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Wang, J.H.
The role of activation-induced deaminase in antibody diversification and genomic instability
Immunol. Res.
55
287-297
2013
Homo sapiens (Q9GZX7), Mus musculus (Q9WVE0)
brenda
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
J. Biol. Chem.
274
18470-18476
1999
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
J. Biol. Chem.
287
21520-21529
2012
Mus musculus (Q9WVE0)
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
J. Exp. Med.
205
2585-2594
2008
Mus musculus (Q9WVE0)
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
Mol. Cell. Biol.
31
442-449
2011
Mus musculus (Q9WVE0)
brenda
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
232-242
2011
Mus musculus (Q9WVE0)
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
438
508-511
2005
Mus musculus (Q9WVE0)
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
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
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