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Updated: Jun 4, 2026

RNA-seq Analysis of Transcriptomes in Thrombin-treated and Control Human Pulmonary Microvascular Endothelial Cells
Published on: February 13, 2013
p38 MAPK controls prothrombin expression by regulated RNA 3' end processing
Sven Danckwardt1, Anne-Susan Gantzert, Stephan Macher-Goeppinger
1Department of Pediatric Oncology, Hematology, and Immunology, University of Heidelberg, Heidelberg, Germany.
Stress and inflammation regulate gene expression post-transcriptionally. This involves p38 MAPK activating proteins that control mRNA processing, impacting blood coagulation and tumor invasion.
Area of Science:
- Molecular Biology
- Biochemistry
- Gene Regulation
Background:
- Thrombin is a critical protease in coagulation, inflammation, and angiogenesis.
- Mechanisms controlling prothrombin expression were previously unclear.
Purpose of the Study:
- To elucidate the post-transcriptional regulation of prothrombin expression.
- To investigate the role of p38 MAPK in this process.
Main Methods:
- Analysis of mRNA 3' end processing.
- Western blotting to detect protein phosphorylation.
- In vivo studies in disease models.
Main Results:
- Prothrombin expression is regulated by a stress- and inflammation-responsive post-transcriptional mechanism.
- p38 MAPK activation leads to phosphorylation of FBP2 and FBP3.
- Phosphorylated FBP2/FBP3 release the upstream sequence element (USE) in 3'UTRs, enabling 3' end processing.
Conclusions:
- Regulated 3' end processing is a key gene regulation mechanism.
- This pathway is implicated in inflammatory hypercoagulation and tumor invasion.
- Discoveries offer insights into broad biological and medical implications.
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