ERK activation is required for CCK-mediated pancreatic adaptive growth in mice.

High levels of cholecystokinin (CCK) can stimulate pancreatic adaptive growth in which mature acinar cells divide, leading to enhanced pancreatic mass with parallel increases in protein, DNA, RNA, and digestive enzyme content. Prolonged release of CCK can be induced by feeding trypsin inhibitor (TI) to disrupt normal feedback control. This leads to exocrine growth in a CCK-dependent manner.

Quantitative glycomics from fluidic glycan microarrays.

A hallmark of cell-surface processes involving glycans is their multivalent interaction with glycan binding proteins (GBPs). Such a multivalent interaction depends critically on the mobility and density of signaling molecules on the membrane surface. While glycan microarrays have been used in exploring multivalent interactions, the lack of mobility and the difficulty in controlling surface density both limit their quantitative applications.

Fluidic and air-stable supported lipid bilayer and cell-mimicking microarrays.

As drug delivery, therapy, and medical imaging are becoming increasingly cell-specific, there is a critical need for high fidelity and high-throughput screening methods for cell surface interactions. Cell membrane-mimicking surfaces, i.e.

Denaturing and refolding of protein molecules on surfaces.

Keeping protein molecules in the active state on a solid surface is essential to protein microarrays and other protein-based biosensors. Here, we show that the 2-D chemical environment controls the refolding of the denatured green fluorescent proteins tethered to solid surfaces. Refolding occurs readily on the repulsive PEG functionalized surface but is inhibited on the attractive--NH(2) functionalized surface.