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Background <p>Cell migration is a fundamental biological process essential for embryonic development and hematopoiesis. In a shRNA screen, we identified the TRAM-LAG1-CLN8 domain-containing transmembrane protein TMEM56 as a previously uncharacterized regulator of stromal cell-derived factor 1 (SDF-1)-mediated cell migration. This study investigates the molecular mechanisms underlying TMEM56 function.</p> Results <p>TMEM56 is expressed in both murine embryonic and adult tissues, with enrichment in hematopoietic stem and erythroid progenitor cells. Lipidomic analysis reveals that TMEM56 modulates ceramide metabolism, particularly affecting levels of hexosylated ceramides. Co-immunoprecipitation assays indicate that TMEM56 physically interacts with ceramide synthase 2 (CerS2), suggesting a role in lipid signaling pathways.</p> Conclusion <p>Our findings identify TMEM56 as a key regulator of cell migration, linking lipid metabolism with hematopoietic and developmental processes. These results provide novel insights into the molecular mechanisms governing migration.</p>

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TRAM-LAG1-CLN8 domain-containing protein TMEM56 regulates cell migration by changing intracellular ceramide levels

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月5日

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  • Benjamin Dorschner,
  • Ralf Wiedemuth,
  • Cornelia Richter,
  • Marc Gentzel,
  • Tobias Lindau,
  • Gunes Ozhan,
  • Gilbert Weidinger,
  • Sebastian Brenner,
  • Sebastian Thieme

摘要

Background

Cell migration is a fundamental biological process essential for embryonic development and hematopoiesis. In a shRNA screen, we identified the TRAM-LAG1-CLN8 domain-containing transmembrane protein TMEM56 as a previously uncharacterized regulator of stromal cell-derived factor 1 (SDF-1)-mediated cell migration. This study investigates the molecular mechanisms underlying TMEM56 function.

Results

TMEM56 is expressed in both murine embryonic and adult tissues, with enrichment in hematopoietic stem and erythroid progenitor cells. Lipidomic analysis reveals that TMEM56 modulates ceramide metabolism, particularly affecting levels of hexosylated ceramides. Co-immunoprecipitation assays indicate that TMEM56 physically interacts with ceramide synthase 2 (CerS2), suggesting a role in lipid signaling pathways.

Conclusion

Our findings identify TMEM56 as a key regulator of cell migration, linking lipid metabolism with hematopoietic and developmental processes. These results provide novel insights into the molecular mechanisms governing migration.