The many faces of the zinc finger protein 335 in brain development and immune system

• Published in: Biomedicine & pharmacotherapy Vol. 165; p. 115257
• Main Authors: Li, Danyang, Quan, Zhenzhen, Ni, Junjun, Li, Hui, Qing, Hong
• Format: Journal Article
• Language: English
• Published: France Elsevier Masson SAS 01.09.2023; Elsevier
• Subjects: Microcephaly; Neural pathogenesis; T cell development; ZNF335; C/EBPβ; TCR; VZ; E; CNS; DN; TrxG; ZNFs; Microcephaly; AP-1; co-IP; Aβ; IFN-γ; PcG; SVZ; cGAS; SP; AD; KO; MCPH; Neural pathogenesis; CRM1; T cell development; CDK5; cGAMP; TNF-α; RTEs; CCR4-NOT; RCD1; EGR-1; STING; ZNF335; NRC
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2023.115257

Zinc finger protein 335 (ZNF335) plays a crucial role in the methylation and, consequently, regulates the expression of a specific set of genes. Variants of the ZNF335 gene have been identified as risk factors for microcephaly in a variety of populations worldwide. Meanwhile, ZNF335 has also been identified as an essential regulator of T-cell development. However, an in-depth understanding of the role of ZNF335 in brain development and T cell maturation is still lacking. In this review, we summarize current knowledge of the molecular mechanisms underlying the involvement of ZNF335 in neuronal and T cell development across a wide range of pre-clinical, post-mortem, ex vivo, in vivo, and clinical studies. We also review the current limitations regarding the study of the pathophysiological functions of ZNF335. Finally, we hypothesize a potential role for ZNF335 in brain disorders and discuss the rationale of targeting ZNF335 as a therapeutic strategy for preventing brain disorders. [Display omitted] •ZNF335 variants were considered as microcephaly risk factors.•ZNF335 was identified as a regulator of T cell development.•The involvement of ZNF335 in neuronal and T cell development across clinical studies.