Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

AID Rat anti-Human, Alexa Fluor 647, Clone: EK2-5G9, BD

Rat Monoclonal Antibody

Manufacturer:  BD Biosciences 565785

Catalog No. BDB565785


Add to cart

Description

Description

The EK2-5G9 monoclonal antibody specifically binds to human Activation-induced cytidine deaminase (AICDA), also known as AID, or Single-stranded DNA cytosine deaminase. AID is an enzyme that preferentially acts upon certain DNA sequence motifs, such as those located in immunoglobulin variable regions, to induce cytidine-to-uracil mutations. AID-induced mutations initiate both somatic hypermutation (SHM) and class switch recombination (CSR) of the immunoglobulin genes in activated B cells during immune responses. While essential for immunoglobulin gene diversification, dysregulated AID activity can result in genomic instability and oncogenic transformation. Originally thought to be B-cell specific, AID now appears to be abnormally expressed in several epithelial cancers. AID may also play roles in DNA demethylation.

Specifications

Specifications

AID
EK2-5G9
Alexa Fluor 647
Aqueous buffered solution containing ≤0.09% sodium azide.
Rat
IgG2b, κ
50μg
Store undiluted at 4°C and protected from prolonged exposure to light. Do not freeze.
Monoclonal
Flow Cytometry, Immunocytochemistry, Immunofluorescence
0.2mg/mL
AID; ARP2; CDA2; HEL-S-284; HIGM2; Cytidine aminohydrolase
Affinity Purified
Human AID (185-198) Peptide
Affinity Chromatography
RUO
Primary
Human
Documents
Provide Content Correction

We continue to work to improve your shopping experience and your feedback regarding this content is very important to us. Please use the form below to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Cancel Submit