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anti-Human AICDA Anticorps:
anti-Mouse (Murine) AICDA Anticorps:
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Human Polyclonal AICDA Primary Antibody pour 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. dans The Journal of biological chemistry 1999
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Human Polyclonal AICDA Primary Antibody pour 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. dans Virology 2015
Human Monoclonal AICDA Primary Antibody pour ELISA, WB - ABIN2477301
Besmer, Market, Papavasiliou: The transcription elongation complex directs activation-induced cytidine deaminase-mediated DNA deamination. dans Molecular and cellular biology 2006
Human Polyclonal AICDA Primary Antibody pour WB - ABIN2477303
Sekas, Paul: Inhibition of carnitine acyltransferase activities by bile acids in rat liver peroxisomes. dans Biochimica et biophysica acta 1992
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Human Polyclonal AICDA Primary Antibody pour 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. dans Clinical immunology (Orlando, Fla.) 2010
Human Polyclonal AICDA Primary Antibody pour ELISA, WB - ABIN408710
Crouch, Li, Takizawa, Fichtner-Feigl, Gourzi, Montaño, Feigenbaum, Wilson, Janz, Papavasiliou, Casellas: Regulation of AID expression in the immune response. dans The Journal of experimental medicine 2007
Human Monoclonal AICDA Primary Antibody pour 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. dans Journal of immunology (Baltimore, Md. : 1950) 2013
patients with AS expressed significantly higher levels of sv2 (Montrer SV2A Anticorps) than HC. TNFi treatment restored the gene expression of the AID variants (FL, sv1, and sv2 (Montrer SV2A Anticorps)) in patients with AS. Therefore pre-existing TNFalpha (Montrer TNF Anticorps)-induced AID expression in B cells may play a role in the pathogenesis of AS.
we reported high AID, low miR (Montrer MLXIP Anticorps)-181b and high miR (Montrer MLXIP Anticorps)-155 expression in de novo adult B-ALL patients. Univariate high AID or low miR (Montrer MLXIP Anticorps)-181b expression was an unfavorable prognostic factor. High AID with low miR (Montrer MLXIP Anticorps)-181b or with low miR (Montrer MLXIP Anticorps)-155 expression is better in predicting unfavorable OS than univariate factor. High AID with low miR (Montrer MLXIP Anticorps)-181b and low miR (Montrer MLXIP Anticorps)-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 (Montrer RELB Anticorps) 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 (Montrer CEBPA Anticorps) not contr (Montrer GATA1 Anticorps)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 (Montrer TNF Anticorps)-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 (Montrer GH1 Anticorps) 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 (Montrer HELLS Anticorps) dynamics of germinal center B cells are mediated by AID.
MMSET (Montrer WHSC1 Anticorps) promotes AICDA-mediated DNA breaks at the donor switch region during immunoglobulin class switch recombination.
findings suggest that activation of Tnf (Montrer TNF Anticorps)-Aicda axis and co-inhibitory signals to T cells in coordination with Th1 (Montrer HAND1 Anticorps)-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 (Montrer MYC Anticorps) 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 (Montrer CEBPA Anticorps) and Gata1 (Montrer GATA1 Anticorps), myeloid/erythroid lineage-specific transcription factors
UNG (Montrer UNG Anticorps) 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 (Montrer CDA Anticorps) and MDR1 (Montrer ABCB4 Anticorps) transduced hematopoietic 32D as well as primary lin(-) cells was proven in the context of Ara (Montrer FOXC1 Anticorps)-C and anthracycline application
there is currently no evidence to support the proposed roles of AID and MBD4 (Montrer MBD4 Anticorps) in active demethylation in zebrafish embryos.
Results provide evidence for a coupled mechanism of 5-methylcytosine (5-meC (Montrer CCL28 Anticorps)) demethylation, whereby 5-meC (Montrer CCL28 Anticorps) deaminase (AID)deaminates 5-meC (Montrer CCL28 Anticorps), followed by thymine base excision by G:T mismatch-specific thymine glycosylase (Mbd4 (Montrer MBD4 Anticorps)), promoted by Gadd45 (Montrer GADD45A Anticorps).[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 (Montrer TET3 Anticorps) dioxygenase was present in the very first embryo stages, in contrast to TET1 (Montrer TET1 Anticorps) 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