Contents
Vol 14, Issue 676
Research Articles
- A peptide of the N terminus of GRK5 attenuates pressure-overload hypertrophy and heart failure
GRK5 does not mediate pathological signaling in the heart if its nuclear translocation is disrupted.
- Inositol 1,4,5-trisphosphate 3-kinase B promotes Ca2+ mobilization and the inflammatory activity of dendritic cells
Inflammatory responses of dendritic cells in vitro and in vivo require IP4 generated by the kinase ITPKB.
Editors' Choice
- A cancerous connection for creatine
Obesity induces adipocytes to release creatine that is used by nearby breast cancer cells to fuel growth.
About The Cover

Online Cover This week features a Research Article that shows that GRK5 does not mediate pathological signaling in the heart after pressure overload if its nuclear translocation in cardiomyocytes is disrupted. The image shows a cross section of a heart from a mouse subjected to pressure overload, which in humans can be caused by hypertension or myocardial infarction. [Image: Coleman et al./Science Signaling]