Advances in the Regulation of Proteins and Genes for Stem Cells

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Stem Cells".

Deadline for manuscript submissions: closed (31 July 2025) | Viewed by 569

Special Issue Editor


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Guest Editor
Center for Genomics and Proteomics & Stem Cell Core Facility, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon 406-840, Republic of Korea
Interests: stem cells; biomarkers; genomics; proteomics; therapeutics
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Special Issue Information

Dear Colleagues,

Advancements in genomics and proteomics have significantly enhanced our understanding of stem cell biology, offering insights into their fundamental properties and potential therapeutic applications.

Genomics involves the comprehensive analysis of an organism’s complete set of DNA, including all of its genes. In stem cell research, genomics has been instrumental in identifying pluripotency markers, understanding differentiation pathways, and ensuring genomic integrity.

Proteomics is the large-scale study of proteins, which are vital to understanding cellular functions. In the context of stem cells, proteomics has facilitated the elucidation of differentiation mechanisms, the identification of post-translational modifications (PTMs), and the development of diagnostic tools.

The convergence of genomics and proteomics in stem cell research has deepened our understanding of stem cell biology, improved the development of differentiation protocols, and enhanced the safety and efficacy of stem cell-based therapies.

Therefore, this Special Issue will summarize the latest genomic and proteomic findings involved in stem cells, both in maintenance and differentiation. The use of genomic and proteomic biomarkers as potential diagnostic markers and therapeutics for the prevention or treatment of intractable diseases will also be addressed.

I look forward to your contributions.

Prof. Dr. Bonghee Lee
Guest Editor

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Keywords

  • stem cells
  • pluripotency
  • differentiation
  • diagnosis
  • therapeutics

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Published Papers (1 paper)

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Research

15 pages, 6702 KiB  
Article
CREB5 Promotes the Proliferation of Neural Stem/Progenitor Cells in the Rat Subventricular Zone via the Regulation of NFIX Expression
by Tao Yu, Hanyue Zhang, Chuang Zhang, Guorui Ma, Tu Shen, Yan Luan and Zhichao Zhang
Cells 2025, 14(16), 1240; https://doi.org/10.3390/cells14161240 - 12 Aug 2025
Viewed by 374
Abstract
Neural stem/progenitor cells (NSPCs) in the subventricular zone (SVZ) of the central nervous system (CNS) are critical for tissue repair following injury or disease. These cells retain the capacity to proliferate, migrate, and differentiate into neurons, astrocytes, and oligodendrocytes, making them a promising [...] Read more.
Neural stem/progenitor cells (NSPCs) in the subventricular zone (SVZ) of the central nervous system (CNS) are critical for tissue repair following injury or disease. These cells retain the capacity to proliferate, migrate, and differentiate into neurons, astrocytes, and oligodendrocytes, making them a promising therapeutic target for neurodegenerative disorders and traumatic injuries. However, the molecular mechanisms regulating their proliferation remain incompletely understood. This study investigates the role of cAMP responsive element-binding protein 5 (CREB5) in the proliferation of rat SVZ-derived NSPCs and elucidates its regulatory mechanism. Using RNA interference, we demonstrated that CREB5 knockdown significantly reduced cell viability, neurosphere formation capacity, and the number of proliferating cells (BrdU- and Ki-67-positive cells) both in vitro and in vivo. In contrast, CREB5 overexpression played opposing roles in cell proliferation. Additionally, alteration of CREB5 expression did not affect apoptosis, as assessed by TUNEL staining, indicating a specific role in proliferation rather than in cell death. Mechanistically, we identified Nuclear Factor One X (NFIX) as a transcriptional target of CREB5. CREB5 binds to the AP-1 site in the NFIX promoter, enhancing its expression. CREB5 knockdown inhibited NFIX expression, while CREB5 overexpression exerted the opposite function. ChIP and luciferase reporter assays further confirmed that CREB5 directly regulates NFIX promoter activity. More importantly, alteration of NFIX expression could reverse the effect of CREB5 on NSPC proliferation. These findings highlight CREB5 as a key regulator of NSPC proliferation through its interaction with NFIX, providing a potential therapeutic target for stem cell-based treatments of CNS disorders. Full article
(This article belongs to the Special Issue Advances in the Regulation of Proteins and Genes for Stem Cells)
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