Scholarlink

<p>Protein kinases regulate protein activity through phosphorylation, and many have been reported to participate in brain development. Among them, serine/threonine-protein kinase 24 (STK24) is believed to influence apoptosis, spinal synaptogenesis, and neuronal migration. Despite its recognized roles, the functions of STK24 in the brain remains insufficiently explored. Here, we present an in vivo study of brain-specific <i>Stk24</i> conditional knockout mice. We investigate the impact of <i>Stk24</i> deletion through histological analysis, behavior assays, and the molecular changes. In our results, <i>Stk24</i> deletion disrupts the hippocampal formation during development and decreased subsequent adult hippocampal neurogenesis whilst neuronal morphology is relatively unaffected. Additionally, <i>Stk24</i>-deficient mice exhibit anxiety-like behavior and altered stress responses, featuring increased hippocampal neuronal activity, dysregulated HPA axis reactivity, and modified expression patterns of glucocorticoid receptor signaling-related genes. In conclusion, our findings highlight the involvement of <i>Stk24</i> in brain development, adult hippocampal neurogenesis, as well as anxiety and stress responses.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Stk24 deficiency causes disrupted hippocampal neurogenesis and anxiety-like behavior in mice

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年4月25日

查看全文
  • Kuan-Yu Wu,
  • Chi-Hui Tsao,
  • Nicole Ching Su,
  • Shin-Meng Deng,
  • Guo-Jen Huang

摘要

Protein kinases regulate protein activity through phosphorylation, and many have been reported to participate in brain development. Among them, serine/threonine-protein kinase 24 (STK24) is believed to influence apoptosis, spinal synaptogenesis, and neuronal migration. Despite its recognized roles, the functions of STK24 in the brain remains insufficiently explored. Here, we present an in vivo study of brain-specific Stk24 conditional knockout mice. We investigate the impact of Stk24 deletion through histological analysis, behavior assays, and the molecular changes. In our results, Stk24 deletion disrupts the hippocampal formation during development and decreased subsequent adult hippocampal neurogenesis whilst neuronal morphology is relatively unaffected. Additionally, Stk24-deficient mice exhibit anxiety-like behavior and altered stress responses, featuring increased hippocampal neuronal activity, dysregulated HPA axis reactivity, and modified expression patterns of glucocorticoid receptor signaling-related genes. In conclusion, our findings highlight the involvement of Stk24 in brain development, adult hippocampal neurogenesis, as well as anxiety and stress responses.