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patients with AS expressed significantly higher levels of sv2 (show SV2A Proteins) than HC. TNFi treatment restored the gene expression of the AID variants (FL, sv1, and sv2 (show SV2A Proteins)) in patients with AS. Therefore pre-existing TNFalpha (show TNF Proteins)-induced AID expression in B cells may play a role in the pathogenesis of AS.
we reported high AID, low miR (show MLXIP Proteins)-181b and high miR (show MLXIP Proteins)-155 expression in de novo adult B-ALL patients. Univariate high AID or low miR (show MLXIP Proteins)-181b expression was an unfavorable prognostic factor. High AID with low miR (show MLXIP Proteins)-181b or with low miR (show MLXIP Proteins)-155 expression is better in predicting unfavorable OS than univariate factor. High AID with low miR (show MLXIP Proteins)-181b and low miR (show MLXIP Proteins)-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 Proteins) 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 Proteins) not contr (show GATA1 Proteins)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 Proteins)-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 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.
MMSET (show WHSC1 Proteins) promotes AICDA-mediated DNA breaks at the donor switch region during immunoglobulin class switch recombination.
findings suggest that activation of Tnf (show TNF Proteins)-Aicda axis and co-inhibitory signals to T cells in coordination with Th1 (show HAND1 Proteins)-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 Proteins) 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 Proteins) and Gata1 (show GATA1 Proteins), myeloid/erythroid lineage-specific transcription factors
UNG (show UNG Proteins) 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 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
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.
TET3 dioxygenase was present in the very first embryo stages, in contrast to TET1 (show TET1 Proteins) 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