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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 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 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 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
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 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 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
patients with AS expressed significantly higher levels of sv2 (show SV2A Antibodies) than HC. TNFi treatment restored the gene expression of the AID variants (FL, sv1, and sv2 (show SV2A Antibodies)) in patients with AS. Therefore pre-existing TNFalpha (show TNF Antibodies)-induced AID expression in B cells may play a role in the pathogenesis of AS.
we reported high AID, low miR (show MLXIP Antibodies)-181b and high miR (show MLXIP Antibodies)-155 expression in de novo adult B-ALL patients. Univariate high AID or low miR (show MLXIP Antibodies)-181b expression was an unfavorable prognostic factor. High AID with low miR (show MLXIP Antibodies)-181b or with low miR (show MLXIP Antibodies)-155 expression is better in predicting unfavorable OS than univariate factor. High AID with low miR (show MLXIP Antibodies)-181b and low miR (show MLXIP Antibodies)-155 expression confers worst prognosis.
Results indicate activation-induced cytidine deaminase (AICDA) as a driver of epigenetic heterogeneity in B-cell lymphomas with potential significance for other tumors with aberrant expression of cytidine deaminases.
The binding and catalytic behavior of purified AID was tested on DNA/RNA hybrid substrates bearing either random sequences or GC-rich (show RELB Antibodies) sequences simulating Ig S regions. AID exhibited a higher affinity for binding DNA/RNA hybrid substrates made of S region sequences, than any other DNA substrates. In the absence of any other cellular processes or factors, AID itself favors binding and mutating S-region DNA/RNA hybrids.
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.
MMSET (show WHSC1 Antibodies) promotes AICDA-mediated DNA breaks at the donor switch region during immunoglobulin class switch recombination.
findings suggest that activation of Tnf (show TNF Antibodies)-Aicda axis and co-inhibitory signals to T cells in coordination with Th1 (show HAND1 Antibodies)-type immunity has critical roles in the immune response against Hepatitis B virus infection
the role of phosphorylation on AID serine38 in AID activity at the Immunoglobulin switch region and off-target Myc (show MYC Antibodies) gene, is reported.
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.
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
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.
TET3 (show TET3 Antibodies) dioxygenase was present in the very first embryo stages, in contrast to TET1 (show TET1 Antibodies) and AICDA.
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.
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 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).
, integrated into Burkitt's lymphoma cell line Ramos
, single-stranded DNA cytosine deaminase
, activation induced deaminase
, activation-induced cytidine deaminase
, activation induced cytidine deaminase
, activation-induced deaminase