Publications by authors named "Julian Brenig"

Article Synopsis
  • The study examined how varying oxygen levels (hypoxia) affect the production of nitric oxide (NO) and deformability of red blood cells (RBCs) in healthy individuals.
  • It was found that RBC-NOS (a type of enzyme) activity decreased with more severe hypoxia, leading to decreased RBC deformability under mild hypoxia but increased deformability under severe hypoxia.
  • The results suggest that non-enzymatic production of NO helps maintain RBC deformability during severe hypoxia, which is crucial for ensuring adequate oxygen delivery to tissues.
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Rho proteins are small GTP/GDP-binding proteins primarily involved in cytoskeleton regulation. Their GTP/GDP cycle is often tightly connected to a membrane/cytosol cycle regulated by the Rho guanine nucleotide dissociation inhibitor α (RhoGDIα). RhoGDIα has been regarded as a housekeeping regulator essential to control homeostasis of Rho proteins.

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Ran is a small GTP-binding protein of the Ras superfamily regulating fundamental cellular processes: nucleo-cytoplasmic transport, nuclear envelope formation and mitotic spindle assembly. An intracellular Ran•GTP/Ran•GDP gradient created by the distinct subcellular localization of its regulators RCC1 and RanGAP mediates many of its cellular effects. Recent proteomic screens identified five Ran lysine acetylation sites in human and eleven sites in mouse/rat tissues.

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Diaphanous-related formins are eukaryotic actin nucleation factors regulated by an autoinhibitory interaction between the N-terminal RhoGTPase-binding domain (mDiaN) and the C-terminal Diaphanous-autoregulatory domain (DAD). Although the activation of formins by Rho proteins is well characterized, its inactivation is only marginally understood. Recently, liprin-α3 was shown to interact with mDia1.

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Background: Nitric oxide (NO) produced by nitric oxide synthase (NOS) in human red blood cells (RBCs) was shown to depend on shear stress and to exhibit important biological functions, such as inhibition of platelet activation. In the present study we hypothesized that exercise-induced shear stress stimulates RBC-NOS activation pathways, NO signaling, and deformability of human RBCs.

Methods/findings: Fifteen male subjects conducted an exercise test with venous blood sampling before and after running on a treadmill for 1 hour.

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