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<p>Acidic nuclear phosphoprotein 32A (ANP32A) is not only a core component of the inhibitor of histone acetyltransferases (INHAT) complex but also a crucial pleiotropic protein regulating cellular homeostasis and disease progression. Its extensive involvement in transcriptional regulation, apoptotic cascades, and signal transduction underpins its pivotal role across virology, neurobiology, and oncology. This review systematically elucidates the structure–function relationship of ANP32A, delineating its role as an essential host factor for viral replication​ and its complex involvement in neurodegenerative processes. Particular emphasis is placed on its context-dependent duality within oncology, where it exerts a pronounced "double-edged sword" effect by acting as either a tumor suppressor or an oncogene depending on the cellular milieu. Ultimately, this article aims to provide a theoretical foundation for the development of precision-targeted clinical interventions directed at ANP32A.</p>

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Acidic nuclear phosphoprotein 32A (ANP32A): structure, function, and its role in disease pathogenesis

  • 期刊论文

  • 发表日期：

    2026年7月20日

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  • Zhiqi Zhang,
  • Enjie Liu,
  • Zeyuan Wang,
  • Yajun Huo,
  • Yifan Shang,
  • Huimin Du,
  • Jun Yu,
  • Wencai Li

摘要

Acidic nuclear phosphoprotein 32A (ANP32A) is not only a core component of the inhibitor of histone acetyltransferases (INHAT) complex but also a crucial pleiotropic protein regulating cellular homeostasis and disease progression. Its extensive involvement in transcriptional regulation, apoptotic cascades, and signal transduction underpins its pivotal role across virology, neurobiology, and oncology. This review systematically elucidates the structure–function relationship of ANP32A, delineating its role as an essential host factor for viral replication​ and its complex involvement in neurodegenerative processes. Particular emphasis is placed on its context-dependent duality within oncology, where it exerts a pronounced "double-edged sword" effect by acting as either a tumor suppressor or an oncogene depending on the cellular milieu. Ultimately, this article aims to provide a theoretical foundation for the development of precision-targeted clinical interventions directed at ANP32A.