Custom-made 15N-enriched CCL21 protein supplied by Protein Foundry The chemokine CCL21 guides both T cell and metastatic cancer homing to lymph nodes by activating the receptor CCR7. CCL21 is among a handful of chemokines with an unstructured
Cloned antibodies from patients with heparin-induced thrombocytopenia (HIT) provide new clues to HIT pathogenesis A recent study published in Blood from scientists at @BloodCenterWI and @MayoClinic reveals structural differences between
When a chemokine binds to its G protein-coupled receptor one of the consequences of receptor activation is a decrease in the levels of receptor present on the cell surface due to more rapid internalization. The mechanism of GPCR internalization
CXCL12 and its receptor CXCR4 have well known roles in bone marrow homing and mobilization of hematopoietic stem cells and neutrophils, but inflammatory neutrophil recruitment is governed by CXCR2 and its
Plasma concentrations of inflammatory proteins can serve as biomarkers for cardiovascular disease (CVD). Previous studies had linked the T cell chemokine CXCL10/IP-10 to hypertension and heart failure, but failed to achieve the statistical significance necessary for its use as a biomarker for human disease.
As reported recently in the Wall Street Journal and other publications, the human chemokine CXCL4 (also known as platelet factor 4 or PF4) is the common link between COVID-19 vaccine-induced immune thrombotic thrombocytopenia (VITT) and a more common condition known as heparin-induced thrombocytopenia (HIT).
A shapeshifting immune system protein called XCL1 evolved from a single-shape ancestor hundreds of millions of years ago. Researchers at the Medical College of Wisconsin discovered the molecular basis for how this happened, in a study
Using a hybrid modeling approach, Fox generated a model for the chemokine XCL1 in complex with its G protein-coupled receptor XCR1 and identified key interaction sites. Changes within a region of XCL1 that determined its binding energy to XCR1 changed the activity of the receptor and, consequently, cell migration