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AICDA encodes a RNA-editing deaminase that is a member of the cytidine deaminase family. Additionally we are shipping AICDA Antibodies (121) and AICDA Kits (1) and many more products for this protein.
Showing 7 out of 11 products:
Human AICDA Protein expressed in Escherichia coli (E. coli) - ABIN1098741
Guo, Su, Zhong, Ming, Song: Hydroxylation of 5-methylcytosine by TET1 promotes active DNA demethylation in the adult brain. in Cell 2011
Show all 2 references for ABIN1098741
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.
this study reports a case of growth hormone (show GH1 Proteins) deficiency with an autosomal recessive Hyper-immunoglobulin M syndrome by phenotype and genotype, with a novel mutation in AICDA that has not been reported formerly
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 Proteins) 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 Proteins) 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 Proteins).
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 Proteins).
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 Proteins) and sustained survival signals in HCV-related CV patients.
Efficient chemoprotection of CDD (show CDA Proteins) and MDR1 (show ABCB4 Proteins) transduced hematopoietic 32D as well as primary lin(-) cells was proven in the context of Ara (show FOXC1 Proteins)-C and anthracycline application
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 Proteins) and the ARP2/3 complex.
Study finds AID targets somatic hypermutation (SHM (show CNTNAP1 Proteins)) hotspots within V exon and S region passengers at similar frequencies and that the normal SHM (show CNTNAP1 Proteins) process frequently generates deletions, indicating that SHM (show CNTNAP1 Proteins) 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 Proteins) inhibitors indirectly target AID in vivo
crystal structure of Arp2 (show ACTR2 Proteins)/3 complex
These results demonstrate an important role for CRMP-1 (show CRMP1 Proteins) in Listeria actin comet tail formation and open the possibility that CRMP-1 (show CRMP1 Proteins) controls cell motility by modulating Arp2 (show ACTR2 Proteins)/3 activation.
TET3 dioxygenase was present in the very first embryo stages, in contrast to TET1 (show TET1 Proteins) 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 Proteins)
Data show that L. monocytogenes motility can be separated into an Arp2 (show ACTR2 Proteins)/3-dependent nucleation phase, and an Arp2 (show ACTR2 Proteins)/3-independent elongation phase which is dependent upon fascin (show FSCN1 Proteins).
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 Proteins) in active demethylation in zebrafish embryos.
Results provide evidence for a coupled mechanism of 5-methylcytosine (5-meC (show CCL28 Proteins)) demethylation, whereby 5-meC (show CCL28 Proteins) deaminase (AID)deaminates 5-meC (show CCL28 Proteins), followed by thymine base excision by G:T mismatch-specific thymine glycosylase (Mbd4 (show MBD4 Proteins)), promoted by Gadd45 (show GADD45A Proteins).[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