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AICDA encodes a RNA-editing deaminase that is a member of the cytidine deaminase family. Additionally we are shipping Activation-Induced Cytidine Deaminase Proteins (8) and Activation-Induced Cytidine Deaminase Kits (5) and many more products for this protein.
Showing 10 out of 127 products:
Human Polyclonal AICDA Primary Antibody for EIA, IF - ABIN499233
Muramatsu, Sankaranand, Anant, Sugai, Kinoshita, Davidson, Honjo: Specific expression of activation-induced cytidine deaminase (AID), a novel member of the RNA-editing deaminase family in germinal center B cells. in The Journal of biological chemistry 1999
Show all 5 references for ABIN499233
Human Polyclonal AICDA Primary Antibody for ELISA, WB - ABIN263175
Crouch, Li, Takizawa, Fichtner-Feigl, Gourzi, Montaño, Feigenbaum, Wilson, Janz, Papavasiliou, Casellas: Regulation of AID expression in the immune response. in The Journal of experimental medicine 2007
Human Polyclonal AICDA Primary Antibody for IF (p) - ABIN881942
Demberg, Mohanram, Musich, Brocca-Cofano, McKinnon, Venzon, Robert-Guroff: Loss of marginal zone B-cells in SHIVSF162P4 challenged rhesus macaques despite control of viremia to low or undetectable levels in chronic infection. in Virology 2015
Features of activation-induced deaminase (AID) mapping within the noncatalytic domain, but outside the chromosome region maintenance 1-dependent nuclear export signal at the C-terminus, influence its function.
AICDA/APOBEC family of cytidine deaminases is significant in innate immunity, as it restricts numerous viruses, including HBV, through hypermutationdependent and independent mechanisms. (Review)
DNA methylation (show HELLS Antibodies) dynamics of germinal center B cells are mediated by AID.
Mutations in activation-induced cytidine deaminase is associated with indolent chronic lymphocytic leukaemia.
Data suggest novel mechanism in innate immunity allows cytokine TGF-beta (show TGFB1 Antibodies) to restrict viral circular DNA in hepatocyte nuclei via innate immunity; AID deaminates circular DNA of hepatitis B virus leading to DNA degradation; mechanism depends on UNG (show UNG Antibodies).
The high levels of memory and activated B cells and follicular helper T cells were positively associated with the progression of immunoglobulin A nephropathy. This may be mediated by the overexpression of AID, which is potentially regulated by IL21 (show IL17C Antibodies).
High expression of activation-induced cytidine deaminase is associated with diffuse large B cell lymphoma.
AID mutations leading to AID deficiency are the most frequent underlying molecular basis of hyper IgM syndrome in consanguineous Tunisian patients.
Studies indicate that gene conversion mediated by activation-induced cytidine deaminase (AID) has been found to contribute to generation of the primary antibody repertoire.
aberrant expression of AID may reflect continuous B cell activation (show BLNK Antibodies) and sustained survival signals in HCV-related CV patients.
Surges in ERK activity induced by extracellular cues enhance Arp2/3-mediated actin polymerization to generate protrusion power phases sufficient to promote sustained cell motility.
Dendritic cells possess a mechanism to pass through micrometric constrictions. This mechanism is based on a rapid Arp2/3-dependent actin nucleation around the nucleus that disrupts the nuclear lamina, the main structure limiting nuclear deformability.
demonstrate that the Arp2/3 complex in higher eukaryotes is actually a family of complexes with different properties
The effect of insertion of transcribed intronic S regions in a locus (Igkappa)strongly recruiting AICDA on class switch recombination is reported.
Platelet actin nodule formation is dependent on WASp (show WASL Antibodies) and the ARP2/3 complex.
Study finds AID targets somatic hypermutation (SHM (show CNTNAP1 Antibodies)) hotspots within V exon and S region passengers at similar frequencies and that the normal SHM (show CNTNAP1 Antibodies) process frequently generates deletions, indicating that SHM (show CNTNAP1 Antibodies) and class-switch recombination employ the same mechanism.
Splice variants of activation induced deaminase (AID) do not affect the efficiency of class switch recombination in murine CH12F3 cells
AID deficiency inhibits DSA-mediated aortic vasculopathy after aorta transplantation in mice.
HSP90 (show HSP90 Antibodies) inhibitors indirectly target AID in vivo
class switch recombination is programmed to occur in a productive deletional orientation and does so via an unprecedented mechanism that involves in cis Igh organizational features in combination with frequent S-region DSBs initiated by AID
crystal structure of Arp2 (show ACTR2 Antibodies)/3 complex
These results demonstrate an important role for CRMP-1 (show CRMP1 Antibodies) in Listeria actin comet tail formation and open the possibility that CRMP-1 (show CRMP1 Antibodies) controls cell motility by modulating Arp2 (show ACTR2 Antibodies)/3 activation.
TET3 (show TET3 Antibodies) dioxygenase was present in the very first embryo stages, in contrast to TET1 (show TET1 Antibodies) and AICDA.
The GMF-Arp2 interface reveals how the ADF-H actin-binding domain in GMF is exploited to specifically recognize Arp2/3 complex and not actin.
interacts with contactin and N-WASp (show WASL Antibodies)
Data show that L. monocytogenes motility can be separated into an Arp2 (show ACTR2 Antibodies)/3-dependent nucleation phase, and an Arp2 (show ACTR2 Antibodies)/3-independent elongation phase which is dependent upon fascin (show FSCN1 Antibodies).
crystal structures of Arp2/3 complex with bound ATP or ADP
WASp stabilizes p35-dependent closure of the complex, holding Arp2 and Arp3 closer together to nucleate an actin filament.
domain rearrangements of Arp2 and Arp3 result in a closed conformational state consistent with an "actin-dimer" model for the active state
AICDA cDNA was cloned and expressed successfully in Escherichia coli generating a phenotype consistent with the mutating action of this deaminase. Using a whole genome radiation hybrid panel, AICDA was mapped to a region of chromosome 5.
there is currently no evidence to support the proposed roles of AID and MBD4 (show MBD4 Antibodies) in active demethylation in zebrafish embryos.
Results provide evidence for a coupled mechanism of 5-methylcytosine (5-meC (show CCL28 Antibodies)) demethylation, whereby 5-meC (show CCL28 Antibodies) deaminase (AID)deaminates 5-meC (show CCL28 Antibodies), followed by thymine base excision by G:T mismatch-specific thymine glycosylase (Mbd4 (show MBD4 Antibodies)), promoted by Gadd45 (show GADD45A Antibodies).[AID]
The promoters of both channel catfish (Ictalurus punctatus) and zebrafish (Danio rerio) Aicda genes were as transcriptionally active as an SV40 promoter control in all cell lines tested, regardless of the cells ability to express Aicda.
This gene encodes a RNA-editing deaminase that is a member of the cytidine deaminase family. The protein is involved in somatic hypermutation, gene conversion, and class-switch recombination of immunoglobulin genes. Defects in this gene are the cause of autosomal recessive hyper-IgM immunodeficiency syndrome type 2 (HIGM2).
activation-induced cytidine deaminase
, activation induced deaminase
, activation-induced deaminase
, cytidine aminohydrolase
, integrated into Burkitt's lymphoma cell line Ramos
, single-stranded DNA cytosine deaminase
, activation induced cytidine deaminase
, ARP2 actin-related protein 2 homolog
, actin-like protein 2
, actin-related protein 2