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A nucleoporin allows nuclear pore complexes access to daughter cell during mitosis.

People & Ideas

Colón-Ramos studies neurodevelopment in C. elegans.


Cell biology in neuroscience


The presence of members of an NPC subcomplex containing Nsp1p is required for NPC movement into a daughter yeast cell, allowing intact NPCs to bypass a filter that prevents movement of defective complexes.

Large, insoluble aggregates of a yeast prion protein are required for the prion phenotype, but soluble oligomers contain all the information necessary to transmit the prion conformation.

Live imaging reveals that muscle microtubules are highly dynamic and build a durable network nucleated by static Golgi elements.


A cytoplasmic pool of Nsp1 is targeted to the bud in a Myo2-dependent manner and is required for nuclear pore complex inheritance by daughter cells.

The Golgi protein RhoBTB3 in complex with CUL3 and RBX1 promotes Cyclin E ubiquitylation to allow its turnover during S phase and progression through the cell cycle.

Positioning of the mitotic spindle relative to the luminal domain in epithelial cells is determined by Par1b in a RhoA-mediated signaling pathway that involves the astral microtubule anchoring complex LGN–NuMA.

β(1,3)glucan is critical for contractile ring positioning and for coupling septum synthesis to constriction of the contractile ring and plasma membrane extension during cytokinesis.

The V0 membrane domain of the V-ATPase reversibly dissociates from V1 at acidic intragranular pH and is necessary for normal exocytosis and synaptic transmission.

Atg38 provides a physical linkage between the Vps15–Vps34 and Atg14–Vps30 subcomplexes to facilitate PI3-kinase complex I formation.

Dynamin 2 is required for starvation-mediated breakdown of lipid droplets in hepatocytes by promoting vesiculation of autolysosomal tubules to release protolysosomes.

FOXO1 orchestrates wound healing through the up-regulation of TGF-β1 and protection against oxidative stress, which together act to promote keratinocyte migration and decrease apoptosis.

The BMP signaling pathway promotes muscle growth and inhibits muscle wasting via SMAD1/5-dependent signaling.

Mathematical modeling and analysis of 3D epithelial structures indicate that epithelial growth can take place far from mechanical equilibrium, depending on cell–cell and cell–ECM contact, cell division, cortical contractility, and cell motility.


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