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Human Polyclonal AICDA Primary Antibody für 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
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Human Polyclonal AICDA Primary Antibody für 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 Polyclonal AICDA Primary Antibody für 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 für 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 Monoclonal AICDA Primary Antibody für 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 für 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 für WB - ABIN2477303
Sekas, Paul: Inhibition of carnitine acyltransferase activities by bile acids in rat liver peroxisomes. in Biochimica et biophysica acta 1992
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we reported high AID, low miR (zeige MLXIP Antikörper)-181b and high miR (zeige MLXIP Antikörper)-155 expression in de novo adult B-ALL patients. Univariate high AID or low miR (zeige MLXIP Antikörper)-181b expression was an unfavorable prognostic factor. High AID with low miR (zeige MLXIP Antikörper)-181b or with low miR (zeige MLXIP Antikörper)-155 expression is better in predicting unfavorable OS than univariate factor. High AID with low miR (zeige MLXIP Antikörper)-181b and low miR (zeige MLXIP Antikörper)-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 (zeige RELB Antikörper) 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 (zeige CEBPA Antikörper) not contr (zeige GATA1 Antikörper)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 (zeige TNF Antikörper)-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 (zeige GH1 Antikörper) 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 (zeige HELLS Antikörper) dynamics of germinal center B cells are mediated by AID.
Mutations in activation-induced cytidine deaminase is associated with indolent chronic lymphocytic leukaemia.
MMSET (zeige WHSC1 Antikörper) promotes AICDA-mediated DNA breaks at the donor switch region during immunoglobulin class switch recombination.
findings suggest that activation of Tnf (zeige TNF Antikörper)-Aicda axis and co-inhibitory signals to T cells in coordination with Th1 (zeige HAND1 Antikörper)-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 (zeige MYC Antikörper) 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 (zeige CEBPA Antikörper) and Gata1 (zeige GATA1 Antikörper), myeloid/erythroid lineage-specific transcription factors
UNG (zeige UNG Antikörper) 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 (zeige CDA Antikörper) and MDR1 (zeige ABCB4 Antikörper) transduced hematopoietic 32D as well as primary lin(-) cells was proven in the context of Ara (zeige FOXC1 Antikörper)-C and anthracycline application
there is currently no evidence to support the proposed roles of AID and MBD4 (zeige MBD4 Antikörper) in active demethylation in zebrafish embryos.
Results provide evidence for a coupled mechanism of 5-methylcytosine (5-meC (zeige CCL28 Antikörper)) demethylation, whereby 5-meC (zeige CCL28 Antikörper) deaminase (AID)deaminates 5-meC (zeige CCL28 Antikörper), followed by thymine base excision by G:T mismatch-specific thymine glycosylase (Mbd4 (zeige MBD4 Antikörper)), promoted by Gadd45 (zeige GADD45A Antikörper).[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 (zeige TET3 Antikörper) dioxygenase was present in the very first embryo stages, in contrast to TET1 (zeige TET1 Antikörper) 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