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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Related Experiment Video

Updated: Mar 7, 2026

Translating Ribosome Affinity Purification TRAP for RNA Isolation from Endothelial Cells In Vivo
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Rap1 in endothelial biology.

Magdalena Chrzanowska-Wodnicka1

  • 1Blood Research Institute, BloodCenter of Wisconsin, Part of Versiti, Milwaukee, Wisconsin.

Current Opinion in Hematology
|February 9, 2017
PubMed
Summary

The small GTPase Rap1 is crucial for stabilizing blood vessels and maintaining endothelial function, particularly nitric oxide release. Understanding Rap1

Area of Science:

  • Endothelial biology
  • Molecular signaling
  • Vascular physiology

Background:

  • Small GTPase Rap1 regulates integrin and cadherin processes.
  • Rap1 is downstream from cAMP-activated Epac in endothelium.
  • Rap1 influences angiogenesis and endothelial barrier function.

Purpose of the Study:

  • To investigate the physiological role of Rap1 in mouse models.
  • To uncover molecular details of endothelial barrier regulation.
  • To understand Rap1's role in vessel development and adult conditions.

Main Methods:

  • In vivo studies using mouse models.
  • Genetic manipulation (double knockout of Rap1 isoforms).
  • Analysis of endothelial barrier function, nitric oxide production, and cell adhesion.

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Main Results:

  • Rap1 is essential for vessel stabilization, not initial formation.
  • Rap1 knockout leads to hemorrhage and embryonic lethality.
  • Rap1 is critical for nitric oxide production and endothelial function post-development.
  • Radil and Afadin mediate Rap1's effects on the endothelial barrier.

Conclusions:

  • Rap1 is vital for nitric oxide release and endothelial function in vivo.
  • Rap1 is a key regulator of endothelial cell shear stress responses and homeostasis.
  • Understanding Rap1 mechanisms may reveal therapeutic targets for vascular diseases.