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Updated: Jul 12, 2025

Generation, Purification, and Characterization of Cell-invasive DISC1 Protein Species
Published on: August 30, 2012
Disco interacting protein 2 homolog A (DIP2A): A key component in the regulation of brain disorders
Baoyuan Zhang1, Xuesong Zhang2, Moussa Omorou3
1Department of Physiology, School of Basic Medicine, Jiamusi University, Jiamusi 154000, Heilongjiang, China; Key laboratory of Microecology-immune Regulatory Network and Related Diseases, School of Basic Medicine, Jiamusi University, Jiamusi 154000, Heilongjiang, China.
Abstract:
Disco Interacting Protein 2 Homolog A (DIP2A) is expressed throughout the body and abundantly expressed in the brain tissue. It is activated by Follistatin-like 1 (FSTL1). Activated DIP2A interacts with several pathways, such as AMPK/mTOR and AKT pathways, to contribute to many biological processes, such as oxidative stress, transcriptional regulation, and apoptosis. Dysregulated DIP2A activation has been implicated in numerous processes in the brain. If the upstream pathways of DIP2A remain globally unexplored, many proteins, including cortactin, AMPK, and AKT, have been identified as its downstream targets in the literature. Recent studies have linked DIP2A to a variety of mechanisms in many types of brain disorders, suggesting that regulation of DIP2A could provide novel diagnostic and therapeutic approaches for brain disorders. In this review, we comprehensively summarized and discussed the current research on DIP2A in various brain disorders, such as stroke, autism spectrum disorders (ASD), Alzheimer's disease (AD), dyslexia, and glioma.
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