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<p><i>Fasl</i>-deficient (gld) mice display an altered bone phenotype, but the underlying molecular mechanisms remain incompletely understood. Here we evaluated the role of FASL in the gene expression profile of osteogenic cells. To this aim, RNA sequencing was performed on calvaria-derived primary cells from wild-type and <i>Fasl</i>-deficient mice that underwent osteogenic differentiation. The outcome dataset (GSE250608) contains gene expression profiles and enrichment analyses. Based on a log2 fold change &gt;1 and adjusted p-value &lt; 0.01, the lack of <i>Fasl</i> revealed 480 up- and 301 down-regulated genes. These signature changes were annotated to extracellular matrix-related pathways and chemokine signalling. This resource provides a publicly available transcriptomic dataset that can be used to better understand the complex role of FASL in bone biology.</p>

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Expression changes in Fasl-deficient calvaria-derived osteoblasts: an RNA-seq analysis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月29日

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  • Adela Kratochvilova,
  • Martina Zapletalova,
  • Reinhard Gruber,
  • Eva Janeckova,
  • Lucia Kytkova,
  • Eva Matalova

摘要

Fasl-deficient (gld) mice display an altered bone phenotype, but the underlying molecular mechanisms remain incompletely understood. Here we evaluated the role of FASL in the gene expression profile of osteogenic cells. To this aim, RNA sequencing was performed on calvaria-derived primary cells from wild-type and Fasl-deficient mice that underwent osteogenic differentiation. The outcome dataset (GSE250608) contains gene expression profiles and enrichment analyses. Based on a log2 fold change >1 and adjusted p-value < 0.01, the lack of Fasl revealed 480 up- and 301 down-regulated genes. These signature changes were annotated to extracellular matrix-related pathways and chemokine signalling. This resource provides a publicly available transcriptomic dataset that can be used to better understand the complex role of FASL in bone biology.