Mitophagy regulates mitochondrial quality and mediates extensive mitochondrial degradation in (patho-)physiological settings and is one of the key components of hypoxic preconditioning which protects the heart from ischemia/reperfusion injury.

Heparan sulfates in the vessel wall bind and regulate signaling from the megakaryocyte/platelet-specific inhibitory receptor G6b-B, a critical regulator of platelet homeostasis.

The interaction between activated αIIbβ3 on platelets and SLC44A2 on circulating neutrophils facilitates neutrophil capture and drives flow-dependent NETosis.

TMEM16F shifts its ion selectivity in response to change of intracellular Ca²⁺, membrane potential and ionic strength.

Ligand binding, force and chemistry combine to control the function of a cell surface receptor.

Estrogen is a systemic factor that promotes hematopoietic regeneration by activating the unfolded protein responses.

In a novel cell-in-cell interaction termed emperipolesis, neutrophils routinely transit through the cytoplasm of bone marrow megakaryocytes to pass surface membrane to newly-generated hybrid platelets.

Libraries of patient-derived tumor organoids are a reliable and scalable model system that can help identify and optimize targeted therapies in a pre-clinical setting.

An intelligent method is developed to morphologically classify platelet aggregates by agonist type, which potentially opens a window on novel clinical diagnostics and therapeutics of thrombotic disorders.

Proteins produced by mast cells modulate the permeability of blood vessels, and may determine whether patients infected with dengue virus develop life-threatening complications.