Monitoring the Secretion and Activity of Alpha-1 Antitrypsin in Various Mammalian Cell Types.

Overexpression of recombinant protein in mammalian cells is widely used for producing biologics, as protein maturation and post-translational modifications are similar to human cells. Some therapeutics, such as mRNA vaccines, target nonnative cells that may contain inefficient secretory machinery. For example, gene replacement therapies for alpha-1 antitrypsin (AAT), a glycoprotein normally produced in hepatocytes, are often targeted to muscle cells due to ease of delivery.

ER chaperones use a protein folding and quality control glyco-code.

N-glycans act as quality control tags by recruiting lectin chaperones to assist protein maturation in the endoplasmic reticulum. The location and composition of N-glycans (glyco-code) are key to the chaperone-selection process. Serpins, a class of serine protease inhibitors, fold non-sequentially to achieve metastable active states.

The Heterogeneous Diffusion of Polystyrene Nanoparticles and the Effect on the Expression of Quorum-Sensing Genes and EPS Production as a Function of Particle Charge and Biofilm Age.

Biofilms are abundantly present in both natural and engineered environmental systems and will likely influence broader particle fate and transport phenomena. While some developed models describe the interactions between nanoparticles and biofilms, studies are only beginning to uncover the complexity of nanoparticle diffusion patterns. With the knowledge of the nanoparticle potential to influence bacterial processes, more systematic studies are needed to uncover the dynamics of bacteria-nanoparticle interactions.

Long-range allostery mediates the regulation of plasminogen activator inhibitor-1 by cell adhesion factor vitronectin.

The serpin plasminogen activator inhibitor 1 (PAI-1) spontaneously undergoes a massive structural change from a metastable and active conformation, with a solvent-accessible reactive center loop (RCL), to a stable, inactive, or latent conformation, with the RCL inserted into the central β-sheet. Physiologically, conversion to the latent state is regulated by the binding of vitronectin, which hinders the latency transition rate approximately twofold. The molecular mechanisms leading to this rate change are unclear.