Jonathan D. Pollock

TL;DR: Gene targeting was used to generate mice with a null allele of the gene involved in X–linked CGD, which encodes the 91 kD subunit of the oxidase cytochrome b, and affected hemizygous male mice lacked phagocyte superoxide production and had an altered inflammatory response in thioglycollate peritonitis.

TL;DR: Rac2-deficient mice were created to define the physiological requirement for two near-identical Rac proteins in hematopoietic cells, and showed significant defects in chemotaxis, in shear-dependent L-selectin-mediated capture on the endothelial substrate Glycam-1, and in both F-actin generation and p38 and p42/p44 MAP kinase activation induced by chemoattractants.

TL;DR: Oligonucleotide competition and antibody disruption studies indicated that these complexes contained the transcription factors Spl and Sp3, and additional cis elements may be required to restrict Rac2 promoter activity to hematopoietic cells expressing the endogenous gene.

TL;DR: Using the catalytic subunit of protein kinase A (PKA) and PKA inhibitors, it was shown that PKA is both necessary and sufficient for the cAMP effect on I CI(Ca), which was inhibited by both type 1 and type 2A protein phosphatases.

TL;DR: The special issue on Biomarkers of Nicotine and Tobacco Dependence as discussed by the authors reviewed the science for precision treatment of nicotine dependence and future opportunities for research on biomarkers for inclusion in tobacco product cessation and switching clinical trials to advance translation.