# DAXX in Metabolic, Aging, and Immune Regulation: Recent Insights

**Authors:** Jie Zhou, Liyan Zhao, Qinhui Tuo

PMC · DOI: 10.3390/cells15050425 · Cells · 2026-02-27

## TL;DR

This paper reviews how DAXX regulates metabolism, aging, and immunity, and its potential as a therapeutic target for related diseases.

## Contribution

The paper systematically summarizes recent insights into DAXX's roles in multiple biological processes and its therapeutic potential.

## Key findings

- DAXX regulates metabolic homeostasis and DNA damage repair through nuclear localization and epigenetic control.
- It modulates immune responses by controlling transcription of immune-related genes.
- DAXX's role in telomere stability and aging suggests it could be a target for clinical interventions.

## Abstract

Death domain-associated protein 6 (DAXX) was originally identified as a key regulator of Fas receptor-mediated apoptosis. Recent studies have found that it plays a central role in many biological processes, such as cell metabolism, aging and immunity. DAXX, through its nuclear localization and epigenetic regulatory capabilities, participates in the maintenance of metabolic homeostasis, DNA damage repair, and telomere stability, and modulates immune responses by regulating the transcriptional programs of immune-related genes. This review systematically summarizes recent studies that reveal in various biological processes, including cell metabolism, aging, and immunity, and explores its potential as a therapeutic target, providing a theoretical basis for the study of related diseases and clinical interventions.

## Linked entities

- **Genes:** DAXX (death domain associated protein) [NCBI Gene 1616]

## Full-text entities

- **Genes:** DAXX (death domain associated protein) [NCBI Gene 1616] {aka BING2, DAP6, EAP1}

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12984578/full.md

## References

161 references — full list in the complete paper: https://tomesphere.com/paper/PMC12984578/full.md

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Source: https://tomesphere.com/paper/PMC12984578