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Updated: May 21, 2026
04:17
Determining the Serum Stability of Human Adenosine Deaminase 1 Enzyme
Published on: September 27, 2024
Activation induced deaminase: how much and where?
Alexandre Orthwein1, Javier M Di Noia
1Institut de Recherches Cliniques de Montréal, Montréal, Québec, H2W 1R7, Canada.
Seminars in Immunology
|June 13, 2012
Summary
Activation induced deaminase (AID) regulates adaptive immunity and B cell function. Its levels and location are controlled by post-translational modifications, balancing beneficial roles and pathological risks like cancer.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- Activation induced deaminase (AID) is crucial for adaptive immunity, driving somatic hypermutation (SHM) and class switch recombination (CSR) in B cells.
- Dysregulation of AID contributes to lymphomagenesis and autoimmune diseases, necessitating tight control over its expression and activity.
- Post-translational modifications significantly influence AID's protein levels and subcellular localization, key to modulating its dual physiological and pathological roles.
Purpose of the Study:
- To review the intricate post-translational mechanisms governing Activation induced deaminase (AID) protein levels and subcellular localization.
- To explore how these mechanisms interact, potentially forming a network or cycle, to determine optimal AID protein concentrations.
- To comparatively analyze AID expression levels in immune responses, cancers, and epigenetic remodeling contexts.
Main Methods:
- Literature review of post-translational regulation of AID.
- Analysis of mechanisms controlling AID protein stability, degradation, and nucleocytoplasmic transport.
- Comparative review of AID expression patterns across different biological contexts.
Main Results:
- Multiple mechanisms regulate AID protein levels, including cytoplasmic chaperones for stability and nuclear proteasomal targeting for degradation.
- Nuclear export and cytoplasmic retention limit genomic access of AID, while specific factors mediate its nuclear import.
- Interplay between these mechanisms may operate as a network or cycle to fine-tune AID activity.
Conclusions:
- Post-translational regulation is critical for balancing AID's essential functions in immunity against its oncogenic potential.
- Understanding the network or cycle of AID regulation provides insights into its role in B cell function, disease, and epigenetic modifications.
- Comparative analysis of AID expression highlights its varied roles beyond adaptive immunity.
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