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

Este producto es parte de AICDA - Activation Induced Cytidine Deaminase
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169€ (20 µg)

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935106861
info@markelab.com
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
Descargar

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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