Sarah Cohen

This study uses a dimerization-dependent fluorescent protein system to induce ER-LD membrane contact sites, showing that artificial tethering increases LD size by facilitating lipid incorporation from the ER.

This study identifies APOE interacting with COX-2 on lipid droplets, showing APOE3 promotes and APOE4 suppresses COX-2 activity and prostaglandin production.

This study shows that tubulin polyglutamylation affects Golgi structure and neurite branching during neuronal development.

The paper maps organelle interactions during neuronal differentiation and identifies the ER-peroxisome axis as critical for lipid metabolism and synaptic function.

The paper identifies an alternative splicing event in PLIN3 that generates a mitochondrial-targeted transcript, PLIN3B, which is unstable and not detectable as endogenous protein.

This study shows that tubulin acetylation regulates lysosomal reformation and organelle interactions during neuronal differentiation by shaping organelle architecture and spatial distribution.

The paper characterizes organelle differences and stress responses between neurons and astrocytes using live-cell imaging and quantitative analysis.

This study shows that APOE4 increases lipid droplet accumulation and alters their composition in microglia, resembling a pro-inflammatory state, and overlaps with AD-associated proteomes.

This study shows TDP-43 pathology activates immune cells in ALS, linking it to immune dysfunction and suggesting immune monitoring as a diagnostic tool.

This paper introduces O2-VAE, an orientation-invariant representation learning method for morphologic profiling of cells and organelles, improving clustering and outlier detection.

The paper identifies and characterizes a reference iPSC line, KOLF2.1J, for standardized use in collaborative studies across multiple differentiation protocols and assays.

The paper assesses the transcriptional response of in vitro innate immune cell models to synthetic amyloid beta and finds no robust response, but identifies LPS and INFγ as better activators of microglia-like cells.

The paper uses quantitative proteomics to study murine embryonic heart development and identifies the mevalonate pathway's role in cardiomyocyte proliferation.