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In Focus

Study reveals how a membrane protein boosts Notch signaling in some daughter cells while suppressing it in others.

People & Ideas

Koehler is investigating the mechanisms of mitochondrial protein and RNA import.



Cells with reduced origin firing have an increased rate of replication fork progression, whereas fork progression is slowed in cells with excess origins.

The loss of the spindle checkpoint protein Bub3 is sufficient to induce aneuploidy and drive tumorigenesis when apoptosis is compromised.


Pol η–dependent DNA synthesis at stalled replication forks during S phase suppresses chronic fragile site instability by preventing checkpoint-blind under-replicated DNA in mitosis.

The planarian chromatin regulator HP1, at least in part acting through increased expression of Mcm5, inhibits differentiation of adult stem cells and triggers their proliferation in response to injury.

IFN-γ induces the interaction of HDAC1 and p53, leading to p53 deacetylation, which facilitates autophagy via Bmf suppression.

In sensory organ precursor cells, Sanpodo can enhance or suppress Notch signaling by promoting interaction with Presenilin or driving receptor internalization, respectively.

Endothelial and epithelial barrier disruptions are detected via local decrease in cellular tension, which are coupled to reactive oxygen species–dependent self-restorative actin remodeling dynamics.

Metalloproteinase-mediated cleavage of EphA2 induces breast tumor cells to shift from collective invasion to single-cell invasion.


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