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Validated All-in-One™ qPCR Primer for AICDA(NM_020661.3) Search again
Product ID:
HQP015565
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AID, ARP2, CDA2, HEL-S-284, HIGM2
Gene Description:
activation induced cytidine deaminase
Target Gene Accession:
NM_020661.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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). [provided by RefSeq].
Gene References into function
- required for somatic hypermutation in the centroblast-like Ramos cells; sufficient to induce somatic hypermutation in hybridoma cells, which represent a later stage of B-cell differentiation that does not normally undergo SHM
- AID mutates E. coli suggesting a DNA deamination mechanism for antibody diversification.
- Internal IgH class switch region deletions are position-independent and enhanced by expression
- Somatic hypermutation of the AID transgene in B and non-B cells
- AID is highly regulated during normal B-cell development & is constitutively expressed in human germinal center B-NHL & in subsets of nongerminal center B-NHL. This constitutive expression may cause illegitimate recombination & somatic mutation in B-NHL.
- Chronic lymphocytic leukemia B cells that express this enzyme display dissociation between class switch recombination and somatic hypermutation
- has the function to induce spontaneous IgM production in B cells
- Activation-induced cytidine deaminase causes transcription-dependent, strand-biased C to U deaminations.
- data suggest that AID-mediated DNA alterations may occur in a variably sized, minor subset of B-CLL cells at any given time.
- Expression of activation-induced cytidine deaminase is confined to B-cell non-Hodgkin's lymphomas of germinal-center phenotype.
- Activation-induced cytidine deaminase plays a crucial role in the induction of DNA breakage during immunoglobulin class switch recombination.
- there is an essential role for the C-terminal domain of AID in CSR that is independent of its cytidine deaminase activity and that is not required for either gene conversion or somatic hypermutation
- AID transcripts, including a splice variant, were common to both unmutated or mutated VH genes in mantle cell lymphoma.
- AID is a nucleocytoplasmic shuttling protein with a bipartite nuclear localization signal and a nuclear export signal in its N and C termini, respectively
- AID expression was associated with the ongoing mutation in follicular lymphoma (FL) fresh cells. Results suggest the switch off of AID expression may start in the B-lineage differentiation stage counterpart of FL after optimizing somatic hypermutation
- expression of AID in 15 Burkitt's lymphoma cell lines by RT-PCR
- Activation-induced cytosine deaminase (AID) is actively exported out of the nucleus but retained by the induction of DNA breaks
- results suggested both AID and APOBEC-1 are equally likely to bind single-stranded DNA or RNA, which has implications for the identification of natural AID targets
- separate domains of AID interact with specific cofactors to regulate these two distinct genetic events in a target-specific way
- AID protein is specifically expressed in normal and transformed germinal center B cells
- wild type AID retains its specificity for mutated hot spot motifs within the confines of a moving transcription bubble while introducing clusters of multiple deaminations predominantly on the nontranscribed strand
- novel mutation found in the gene encoding for activation-induced cytidine deaminase in a Tunisian family with hyper-IgM type 2 syndrome
- Aid and perhaps some of its family members may have roles in epigenetic reprogramming
- AID overexpression by itself does not automatically lead to the onset of a mutator phenotype.
- expression in acute lymphoblastic leukemia L2 with t(14;18)(q32;q21)
- Direct evidence is presented for the DNA deamination from Escherichia coli expressing AID; uracils are preferentially generated at cytosines in the nontranscribed strand during transcription.
- AID-mediated deamination of DNA is a major cause of mutations at G-C base pairs in immunoglobulin genes during somatic hypermutation. Its intrinsic substrate specificity is a primary determinant of mutational hotspots at G-C base pairs during SHM.
- AID can interact with MDM2, an oncoprotein that shuttles between the nucleus and the cytoplasm and targets p53 for nuclear export and degradation.
- interfollicular large B cells and AID-expressing B lymphocytes of the thymic medulla could give rise to mature B-cell malignancies.
- Somatic hypermutation on both DNA strands is the natural outcome of AID action on a transcribed gene.
- control of T cell-dependent immune responses may be modulated, via AID, by signals that activate protein kinase A
- The distribution of nuclear AID is consistent with the topography of somatic hypermutation and class switch recombination in activated B cells.
- The AID expression and ASHM are associated with higher-grade transformation of CLL and provide further evidences that AID expression and ASHM may be activated during the clonal history of B-cell lymphomas.
- review of the role of AICDA in producing high affinity isotype-switched antibodies [review]
- a specific domain is required for dimerization of activation-induced cytidine deaminase
- AID binds DNA exposed by the transcribing polymerase, implicating the polymerase itself as the vehicle which distributes AID on DNA as it moves away from the promoter.
- 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.
- APOBEC3G is not a nucleo-cytoplasmic shuttling protein like APOBEC-1 and AID
- AID may persist on immunoglobulin and other target sequences after deamination, possibly acting as a scaffolding protein to recruit other factors
- Findings suggest that the aberrant expression of AID is observed in human hepatocytes with several pathological settings, including chronic liver disease and hepatocellular carcinoma.
- cells may be the founder cells of the germinal center reaction (a pro-GC cell) and may be the normal counterpart of the mantle cell lymphoma cell
- AID is alone unable to act processively on any of a number of DNA substrates
- AID is a BCR-ABL1-induced mutator in Philadelphia chromosome(+) acute lymphoblastic leukemia cells, which may be relevant to the particularly unfavorable prognosis of this leukemia subset.
- primary mediastinal B-cell lymphoma (PMBL), an immunoglobulin (Ig)-negative lymphoma that possesses hypermutated, class-switched Ig genes, expresses high levels of AID with an intact primary structure but does not do class switch recombination
- AID retains its exclusive association with numerous, residual germinal centers in parotid Sjogren's syndrome-MALT lymphomas, whereas neoplastic marginal zone-like B cells are consistently AID negative
- generation of phase 1 mutations is not a prerequisite for the expression of phase 2 mutations
- The proinflammatory cytokine-induced aberrant production of AID might link bile duct inflammation to an enhanced genetic susceptibility to mutagenesis, leading to cholangiocarcinogenesis
- aberrant AID expression can be triggered by several pathogenic factors, including Helicobacter pylori infection & proinflammatory cytokines, in human epithelial cells, but AID expression is absent in those cells under physiologic conditions[review].
- results obtained with activated CD19(+) B cells show that the expression of E47, activation-induced cytidine deaminase, and Iggamma1 circle transcripts progressively decrease with age
- Aberrant expression of activation-induced cytidine deaminase may contribute to the development of gastric cancers and induce p53 nuclear expression
- analysis of the effect of phosphorylation and phosphorylation-null mutants on the activity and deamination specificity of activation-induced cytidine deaminase
- The results, therefore, identify residues in AID involved in its in vivo targeting and suggest they might act through interaction with CTNNBL1, giving possible insight into the linkage between AID recruitment and target-gene transcription.
- Results identify non-conservative homologous recombination as a novel DNA transaction pathway promoted by activation-induced cytidine deaminase.
- AID can cause single-base substitutions or multiple clustered mutations depending on the transcriptional activity of T7 RNA polymerase.
- results lead to a model for exonuclease 1 function in class switch recombination in which cleavage at activation-induced deaminase (AID)-initiated nicks produces gaps that become substrates for further attack by AID and subsequent repair
- V(H)4 replacement in preimmune human B cells is mediated by an AICDA-independent mechanism resulting from inefficient but selective RAG activity.
- Estrogen regulates gene expression of AID at the transcriptional level.