2 research outputs found
Sustainable polycarbonate adhesives for dry and aqueous conditions with thermoresponsive properties
Pressure sensitive adhesives are ubiquitous in commodity products such as tapes, bandages, labels, packaging, and insulation. With single use plastics comprising almost half of yearly plastic production, it is essential that the design, synthesis, and decomposition products of future materials, including polymer adhesives, are within the context of a healthy ecosystem along with comparable or superior performance to conventional materials. Here we show a series of sustainable polymeric adhesives, with an eco-design, that perform in both dry and wet environments. The terpolymerization of propylene oxide, glycidyl butyrate, and CO2, catalyzed by a cobalt salen complex bearing a quaternary ammonium salt, yields the poly(propylene-co-glycidyl butyrate carbonate)s (PPGBC)s. This polymeric adhesive system, composed of environmentally benign building blocks, implements carbon dioxide sequestration techniques, poses minimal environmental hazards, exhibits varied peel strengths from scotch tape to hot-melt wood-glue, and adheres to metal, glass, wood, and Teflon® surfaces.Published versio
CRISPR/Cas9-based editing of a sensitive transcriptional regulatory element to achieve cell type-specific knockdown of the NEMO scaffold protein
The use of alternative promoters for the cell type-specific expression of a given mRNA/protein is a common cell strategy. NEMO is a scaffold protein required for canonical NF-κB signaling. Transcription of the NEMO gene is primarily controlled by two promoters: one (promoter B) drives NEMO transcription in most cell types and the second (promoter D) is largely responsible for NEMO transcription in liver cells. Herein, we have used a CRISPR/Cas9-based approach to disrupt a core sequence element of promoter B, and this genetic editing essentially eliminates expression of NEMO mRNA and protein in 293T human kidney cells. By cell subcloning, we have isolated targeted 293T cell lines that express no detectable NEMO protein, have defined genomic alterations at promoter B, and do not support activation of canonical NF-κB signaling in response to treatment with tumor necrosis factor. Nevertheless, noncanonical NF-κB signaling is intact in these NEMO-deficient cells. Expression of ectopic wildtype NEMO, but not certain human NEMO disease mutants, in the edited cells restores downstream NF-κB signaling in response to tumor necrosis factor. Targeting of the promoter B element does not substantially reduce NEMO expression (from promoter D) in the human SNU423 liver cancer cell line. Thus, we have created a strategy for selectively eliminating cell typespecific expression from an alternative promoter and have generated 293T cell lines with a functional knockout of NEMO. The implications of these findings for further studies and for therapeutic approaches to target canonical NF-κB signaling are discussed.Published versio