Science Signaling

The cBioPortal enables integration, visualization, and analysis of multidimensional cancer genomic and clinical data.

Apoptotic endothelial cells release microRNA-containing microvesicles to modulate the responses of neighboring cells and reduce atherosclerosis in mice.

The gaseous messenger hydrogen sulfide regulates target proteins through S-sulfhydration of cysteine residues.

Reactive oxygen species produced by RBOHD mediate rapid, long-distance stress signals in plants.

The small ubiquitin-like modifier protein SUMO is redistributed among many targets to mediate both short- and long-term signaling events.

Over the past 20 years, the tissue inhibitors of metalloproteinases (TIMPs) have been implicated in direct regulation of cell growth and apoptosis. However, the mechanisms of these effects have been controversial. Recent work by several laboratories has identified specific signaling pathways and cell surface binding partners for members of the TIMP family. TIMP-2 binding to the integrin α ₃ β ₁ is the first description of a cell surface receptor for a TIMP family member. TIMP-2 has been shown to induce gene expression, to promote G ₁ cell cycle arrest, and to inhibit cell migration. TIMP-1 binding to CD63 inhibits cell growth and apoptosis. These new findings suggest that TIMPs are multifunctional and can act either directly through cell surface receptors or indirectly through modulation of protease activity to direct cell fate. The emerging concept is that TIMPs function in a contextual fashion so that the mechanism of action depends on the tissue microenvironment.

Created with both in vitro and in vivo data, NetPhorest is an atlas of consensus sequence motifs for 179 kinases and 104 phosphorylation-dependent binding domains and reveals new insight into phosphorylation-dependent signaling.

Nitric oxide, carbon monoxide, and hydrogen sulfide act as messengers in the cardiovascular, immune, and nervous systems.

Experimental and computational analyses identify multiple cell populations during the epithelial-to-mesenchymal transition.

Regulation of the ubiquitination of Beclin-1 may be a general mechanism that controls autophagy.