Journal: Journal for Immunotherapy of Cancer

Article Title: CD79A/CD40 intracellular domain uses a 4-1BB-like metabolic pathway driven by cholesterol biosynthesis

doi: 10.1136/jitc-2025-012309

Figure Lengend Snippet: Serum LDL cholesterol levels correlate with CAR-T proliferation in the late phase of 4-1BB CAR-T therapy. ( A ) CD3 + CAR-T count in PB of 4-1BB type CAR-T (tisagenlecleucel and lisocabtagene maraleucel) recipients on day 7. ( B ) CD4 + CAR-T count in PB on day 7. ( C ) CD8 + CAR-T count in PB on day 7. ( D ) CD3 + CAR-T count in PB on day 28. ( E ) CD4 + CAR-T count in PB on day 28. ( F ) CD8 + CAR-T count in PB on day 28. ( G ) Effects of lovastatin on CAR-T cell expansion 10 days after Nalm6 stimulation. ( H ) BODIPY-cholesterol uptake on CAR-T 10 days after Nalm6 stimulation. ( I ) LDL receptor MFI on CAR-T 7 days after Nalm6 stimulation. Data were a summary of four healthy human donors and plotted as mean±SEM; *p<0.05, **p<0.01; significance was determined by one-way ANOVA. ANOVA, analysis of variance; LDL, low-density lipoprotein; MFI, median fluorescence intensity; PB, peripheral blood.

Article Snippet: For the cholesterol biosynthesis inhibition assay, CAR-T cells were co-cultured with γ-irradiated Nalm6 cells at a 1:5 responder-to-stimulator ratio in the presence of 10 μM lovastatin (Selleck).

Techniques: Fluorescence

Journal: Nature Communications

Article Title: A fungal tolerance trait and selective inhibitors proffer HMG-CoA reductase as a herbicide mode-of-action

doi: 10.1038/s41467-022-33185-0

Figure Lengend Snippet: a Representative images from the post-emergence treatment of a model dicot, A. thaliana , and pre-emergence treatment of the monocot E. tef , with statins: rosuvastatin (Ro.), pravastatin (Pr.), simvastatin (Si.), mevastatin (Me.), lovastatin (Lo.), fluvastatin (Fl.), atorvastatin (At.) and pitavastatin (Pi.). b A . thaliana (green) and E . t ef (grey) treated with a range of statins at 62.5 μM pre- (light colour) and post-emergence (dark colour) on soil. Inhibition was quantified using a green pixel area and plotted as a percentage of no-inhibitor control. n = 3 replicates with the mean ± standard deviation (s.d.). Source data are provided as a Source Data file.

Article Snippet: Treatments were conducted with rosuvastatin, simvastatin, fluvastatin, atorvastatin (AK Scientific), pravastatin (BOC Sciences), lovastatin (Sapphire Bioscience), mevastatin, pitavastatin (Focus Bioscience), glyphosate, RoundUp® and atorvastatin analogues ( – 9 ).

Techniques: Inhibition, Control, Standard Deviation

Journal: Nature Communications

Article Title: A fungal tolerance trait and selective inhibitors proffer HMG-CoA reductase as a herbicide mode-of-action

doi: 10.1038/s41467-022-33185-0

Figure Lengend Snippet: a The hydrophobic pocket in AtHMG1 delineated by labelled residues (blue sticks) with pitavastatin (magenta sticks) bound, illustrating L558 proximity to the hydrophobic ring of statins. b AtHMG1 with the L558T mutation (grey bar) in comparison to wild-type (black bar) retained activity in vitro in the presence of statins: rosuvastatin (Ro.), pravastatin (Pr.), simvastatin (Si.), mevastatin (Me.), lovastatin (Lo.), fluvastatin (Fl.), atorvastatin (At.) and pitavastatin (Pi.), at 500 nM. n = 3 independent reactions with the mean ± s.d. c In vitro inhibition of WT (black plot) and L558T AtHMG1 (grey plot) by rosuvastatin revealed the L558T mutation conferred >20-fold resistance. n = 3 independent reactions with the mean ± s.d. Source data are provided as a Source Data file.

Article Snippet: Treatments were conducted with rosuvastatin, simvastatin, fluvastatin, atorvastatin (AK Scientific), pravastatin (BOC Sciences), lovastatin (Sapphire Bioscience), mevastatin, pitavastatin (Focus Bioscience), glyphosate, RoundUp® and atorvastatin analogues ( – 9 ).

Techniques: Mutagenesis, Comparison, Activity Assay, In Vitro, Inhibition