Deletion of sphingosine 1-phosphate receptor 1 in myeloid cells reduces hepatic inflammatory macrophages and attenuates MASH.

Background: Immune cell-driven inflammation is a key mediator of metabolic dysfunction-associated steatohepatitis (MASH) progression. We have previously demonstrated that pharmacological sphingosine 1-phosphate (S1P) receptor modulation ameliorates MASH and is associated with attenuated accumulation of intrahepatic macrophage and T-cell subsets. Although S1P receptors are expressed on several immune cell types, given the prominent role of monocyte-derived recruited macrophages in the sterile inflammation of MASH, we hypothesized that deletion of S1P receptor 1 (S1P1) on myeloid cells may ameliorate MASH by reducing the accumulation of proinflammatory monocyte-derived macrophages in the liver.

Towards assembling functional cyanobacterial β-carboxysomes in Oryza sativa chloroplasts.

The major limiting factor of photosynthesis in C3 plants is the enzyme, rubisco which inadequately distinguishes between carbon dioxide and oxygen. To overcome catalytic deficiencies of Rubisco, cyanobacteria utilize advanced protein microcompartments, called the carboxysomes which envelopes the enzymes, Rubisco and Carbonic Anhydrase (CA). These microcompartments facilitate the diffusion of bicarbonate ions which are converted to CO by CA, following in an increase in carbon flux near Rubisco boosting CO fixation process.