M. Kahn | Semantic Scholar

It is reported that thrombin responses in platelets from PAR3-deficient mice were markedly delayed and diminished but not absent, and the identification of a two-receptor system for platelet activation byThrombin has important implications for the development of antithrombotic therapies.

It is reported that in mice with the melanopsin gene ablated, RGCs retrograde-labeled from the suprachiasmatic nuclei were no longer intrinsically photosensitive, although their number, morphology, and projections were unchanged.

Cl cloning and characterization of a new human thrombin receptor, designated protease-activated receptor 3 (PAR3) is reported, which can mediate throm-bin-triggered phosphoinositide hydrolysis and is expressed in a variety of tissues, making it a candidate for the sought-after second platelet throm bin receptor.

Observations suggest that PAR1 and PAR4 account for most, if not all, thrombin signaling in platelets and that antagonists that block these receptors might be useful antithrombotic agents.

It is shown that although disruption of the thrombin receptor (tr) gene in mice causes about half of the tr-/- embryos to die at embryonic day 9–10, half survive to become grossly normal adult mice with no bleeding diathesis.

It is demonstrated that platelets regulate lymphatic vascular development by directly interacting with lymphatic endothelial cells through C-type lectin-like receptor 2 (CLEC-2) receptors, identifying platelets as the cell type in which SLP-76 signaling is required to regulate lymphatics vascular development.

Its expression by cells and tissues not normally exposed to pancreatic trypsin suggests that other proteases could serve as physiological activators and PAR-2 may serve as aTrypsin sensor in the gut.

A hematopoietic signaling pathway required for separation of the two major vascular networks in mammals is revealed, and blood-lymphatic connections lead to embryonic hemorrhage and arteriovenous shunting.

STKs are identified as essential downstream effectors of CCM signaling in development and disease that may regulate both endothelial and epithelial cell junctions and stk deficiency and combined low-level deficiency of stks and ccm3 in zebrafish embryos.