Activation-Induced Cytidine Deaminase (AICDA) Antibody (HRP)

169€ (20 µg)
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935106861
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name
Activation-Induced Cytidine Deaminase (AICDA) Antibody (HRP)
category
Primary Antibodies
provider
Abbexa
reference
abx312572
tested applications
ELISA
Description
AICDA Antibody (HRP) is a Rabbit Polyclonal against AICDA conjugated to HRP.
Documents del producto
Instrucciones
Data sheet
Product specifications
Category | Primary Antibodies |
Immunogen Target | Activation-Induced Cytidine Deaminase (AICDA) |
Host | Rabbit |
Reactivity | Human |
Recommended Dilution | Optimal dilutions/concentrations should be determined by the end user. |
Clonality | Polyclonal |
Conjugation | HRP |
Isotype | IgG |
Purity | > 95% |
Purification | Purified by Protein G. |
Size 1 | 20 µg |
Size 2 | 50 µg |
Size 3 | 100 µg |
Size 4 | 200 µg |
Size 5 | 1 mg |
Form | Liquid |
Tested Applications | ELISA |
Buffer | 0.01 M PBS, pH 7.4, 0.03% Proclin-300 and 50% Glycerol. |
Availability | Shipped within 5-10 working days. |
Storage | Aliquot and store at -20°C. Avoid exposure to light. Avoid repeated freeze/thaw cycles. |
Dry Ice | No |
UniProt ID | Q9GZX7 |
Gene ID | 57379 |
NCBI Accession | NP_001317272.1 |
OMIM | 605257 |
Alias | AID,ARP2,CDA2,HIGM2 |
Background | Antibody anti-AICDA |
Status | RUO |
Descripción
Activation-induced cytidine deaminase (AICDA) is an enzyme crucial for the adaptive immune system, specifically in antibody diversification processes. AICDA is primarily expressed in activated B cells within germinal centers and is a key mediator of somatic hypermutation (SHM) and class switch recombination (CSR) in immunoglobulin genes. Through its enzymatic activity, AICDA deaminates cytidine residues in single-stranded DNA, converting them into uracil during transcription, which introduces mutations or facilitates recombination. This targeted mutagenesis is essential for generating high-affinity antibodies and diversifying antibody classes, enabling the immune system to respond effectively to a wide range of antigens. Dysregulation or mutations in AICDA have been linked to immunodeficiency disorders, such as hyper-IgM syndrome, and its aberrant activity is implicated in genomic instability, contributing to oncogenic mutations in lymphomas. AICDA expression is tightly regulated by transcription factors, including E2F and NF-κB, and is further controlled by post-translational modifications such as phosphorylation. Understanding the precise mechanisms of AICDA function and regulation remains critical, as its activity represents both a cornerstone of adaptive immunity and a potential contributor to mutagenesis in malignancies. Researchers continue to explore AICDA as a target for therapeutic intervention in autoimmune diseases and cancer.
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