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miR-29b acts to silence premature AID expression in naive B cells.
Study demonstrates that AID enters the nucleus in brief pulses, of about 30 min duration. They are independent of AID catalytic activity. AID nuclear accumulation stimulates nuclear accumulation of P53, but while AID appears to be purged from the nucleus at the end of each pulse, nuclear P53 persists in cells that have pulsed. These results identify a new pathway of AID regulation.
Activation induced cytidine deaminase (AID) expression correlated with shorter progression-free survival and overall survival.
AICDA targets SUV4-20-mediated histone H4K20 trimethylation to class-switch recombination sites.
Functional analysis of AID splice variants revealed loss of their activity with respect to SHM, CSR, and induction of double-strand DNA breaks. In silico modeling provided insight into the molecular interactions and structural dynamics of wild-type AID and a shortened AID variant closely resembling AIDDeltaE4, confirming its loss-of-function phenotype.
this study reports the clinical and AID genetic features of six Iranian hyper IgM syndrome patients
induction of AID expression would result in chromosomal translocations in the process of differentiation from B cell derived induced pluripotent stem cells.
The distribution of AID and A3s in the epithelial cells as well as germinal centres.
patients with AS expressed significantly higher levels of sv2 than HC. TNFi treatment restored the gene expression of the AID variants (FL, sv1, and sv2) in patients with AS. Therefore pre-existing TNFalpha-induced AID expression in B cells may play a role in the pathogenesis of AS.
we reported high AID, low miR-181b and high miR-155 expression in de novo adult B-ALL patients. Univariate high AID or low miR-181b expression was an unfavorable prognostic factor. High AID with low miR-181b or with low miR-155 expression is better in predicting unfavorable OS than univariate factor. High AID with low miR-181b and low miR-155 expression confers worst prognosis.
AID expression was increased in chronic lymphocytic leukemia patients with del17p or del11q who have poor 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 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.
Expression of human AID or increased oxidative stress induces DNA breaks within human chromosomal translocation fragile zones.
Data implicate intrinsic preference of AID for structured substrates and uncover the importance of G4 recognition and oligomerization of AID in class switch recombination.
the His130Pro mutation allows the enzyme to retain its mutagenic activity and would prevent the interaction of AID with specific cofactors required for class switch recombination but not for somatic hypermutation. Thus, there would be no contradiction between maintaining the catalytic and mutagenic activity of AID and the presence of function defects at the genomic level.
The authors found that the viral epsilon RNA and C-terminus of AID are required for AID-mediated hepatitis B virus RNA reduction.
silencing of AID in human bone marrow cells skews differentiation toward myelomonocytic lineage. However, in contrast to Tet2 loss, Aid loss does not contribute 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
AID protein is expressed in a large proportion of Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia cases at levels detectable by immunohistochemistry.
These data, showing the direct targeting and induction of functional AID by EBNA3C, suggest a novel role for EBV in the etiology of B cell cancers, including endemic Burkitt lymphoma
PTEN regulated activation-induced cytidine deaminase transcription in germinal center B cells is essential for the class-switch recombination and IgG antibody responses
These data establish a novel link between AID mutagenic activity and lymphomagenesis.
Findings support the notion of a targeting mechanism for the selective diversification of antibody genes with limited genome wide mutagenesis by recruitment of Activation-induced cytidine deaminase by PAX5 and ETS1 in a transcription factor complex.
AID has a role in transcription elongation for mutagenesis in B cells
MMSET promotes AICDA-mediated DNA breaks at the donor switch region during immunoglobulin class switch recombination.
findings suggest that activation of Tnf-Aicda axis and co-inhibitory signals to T cells in coordination with Th1-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 gene, is reported.
Class switching correlates with replication origin activation in immunoglobulin genes;R loops contribute to the specification of origins of replication; Origin activation is independent of AID and DNA breaks
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 and Gata1, myeloid/erythroid lineage-specific transcription factors
UNG 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 and MDR1 transduced hematopoietic 32D as well as primary lin(-) cells was proven in the context of Ara-C and anthracycline application
this study indicate that inflammation-induced AID expression promotes skin cancer development independently of UV damage and suggest AID as a potential target for skin cancer therapeutics.
Molecular mechanism of Aid interaction with RNA-binding proteins, dimer formation and it's role in DNA-cleavage and recombination
DNA methylation dynamics of germinal center B cells are mediated by AID.
Demonstrate the importance of AID in generating an appropriate B1a cell response to pathogenic bacteria.
there is currently no evidence to support the proposed roles of AID and MBD4 in active demethylation in zebrafish embryos.
Results provide evidence for a coupled mechanism of 5-methylcytosine (5-meC) demethylation, whereby 5-meC deaminase (AID)deaminates 5-meC, followed by thymine base excision by G:T mismatch-specific thymine glycosylase (Mbd4), promoted by Gadd45.[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.
The study reports that zebrafish AID was unique among all orthologs in that it efficiently deaminates methylated cytidines.
TET3 dioxygenase was present in the very first embryo stages, in contrast to TET1 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