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anti-Human AICDA Antibodies:
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Human Polyclonal AICDA Primary Antibody for ICC, ELISA - ABIN1001736
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 4 Pubmed References
Human Polyclonal AICDA Primary Antibody for WB - ABIN1882742
Ito, Murakami, Suzuki, Mochida, Suzuki, Ikebuchi, Yamaguchi, Mizuochi: Enhanced expression of lymphomagenesis-related genes in peripheral blood B cells of chronic hepatitis C patients. in Clinical immunology (Orlando, Fla.) 2010
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
Human Polyclonal AICDA Primary Antibody for ELISA, WB - ABIN408710
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 Monoclonal AICDA Primary Antibody for ELISA, WB - ABIN2477301
Besmer, Market, Papavasiliou: The transcription elongation complex directs activation-induced cytidine deaminase-mediated DNA deamination. in Molecular and cellular biology 2006
Human Polyclonal AICDA Primary Antibody for WB - ABIN2477303
Sekas, Paul: Inhibition of carnitine acyltransferase activities by bile acids in rat liver peroxisomes. in Biochimica et biophysica acta 1992
Show all 3 Pubmed References
Human Monoclonal AICDA Primary Antibody for IF, IP - ABIN2668532
Cortizas, Zahn, Hajjar, Patenaude, Di Noia, Verdun: Alternative end-joining and classical nonhomologous end-joining pathways repair different types of double-strand breaks during class-switch recombination. in Journal of immunology (Baltimore, Md. : 1950) 2013
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.
silencing of AID in human bone marrow cells skews differentiation toward myelomonocytic lineage. However, in contrast to Tet2 loss, Aid loss does (show CEBPA Antibodies) not contr (show GATA1 Antibodies)ibute to enhanced HSC self-renewal or cooperate with Flt3-ITD to induce myeloid transformation. Genome-wide transcription and differential methylation analysis uncover the critical role of Aid as a key epigenetic regulator
These findings indicated that TNF-alpha (show TNF Antibodies)-induced AID expression is involved with class switch recombination in cancer.
Finnish founder allele causing HIGM2 identified.
this study reports a case of growth hormone (show GH1 Antibodies) 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 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.
The reduced expression of activation-induced cytidine deaminase (AID).
this study shows that enforced expression of Sox2 in splenic B cells severely inhibits AID expression and IgH class switch recombination
Aid loss in mice leads to expansion of myeloid cells and reduced erythroid progenitors resulting in anemia, with dysregulated expression of Cebpa (show CEBPA Antibodies) and Gata1 (show GATA1 Antibodies), myeloid/erythroid lineage-specific transcription factors
UNG (show UNG Antibodies) deficiency reduces B cell clonal expansion in the germinal center in mice and blocks the proliferation of tumor B cells expressing AID.
We find that the expression of the actin polymerization complex Arp2/3 is reduced in dysbindin-deficient cells, thus affecting actin-dependent phenotypes
Arp2 and Arp3 (show ANGPTL6 Antibodies) expression was increased under atherosclerotic conditions both in ApoE (show APOE Antibodies)-/- mice and in oxidized low-density lipoproteins stimulated human coronary artery endothelial cells (HCAECs).
Efficient chemoprotection of CDD (show CDA Antibodies) and MDR1 (show ABCB4 Antibodies) transduced hematopoietic 32D as well as primary lin(-) cells was proven in the context of Ara (show FOXC1 Antibodies)-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
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 PLURAL_@8014@)
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