Universiteit Leiden

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This Week's Discoveries | 23 May 2017

dinsdag 23 mei 2017
Niels Bohrweg 2
2333 CA Leiden
De Sitterzaal

First lecture

The physical conditions of the cold atomic gas in our Milky Way through very low frequency recombination

Raymond Oonk (Leiden Observatory)
Raymond is a post-doctoral researcher at Leiden Observatory and the Netherlands Institute for Radio Astronomy (ASTRON), working with Huub Rottgering and Xander Tielens. He is interested in studying the interstellar and intergalactic gaseous medium through high resolution line spectroscopy, for example, recombination lines from Carbon and hydrogen in the low frequency radio domain.

The Dutch-led Low Frequency Array (LOFAR) has opened up the low frequency sky (10-270 MHz) at unprecedented sensitivity and resolution.

We utilize these unique capabilities to characterize the physical conditions of the cold, atomic gas in our own Galaxy and beyond. I will show our recent results for the line of sight towards the famous supernova remnant Cassiopeia A and will then briefly discuss these results in the context of our ongoing Galactic survey.

Second lecture

HERG1 channels and integrins in cancer progression

Stefano Coppola (LION)
Stefano is an AXA Research Fund Postdoctoral Fellow in the Physics of Life Processes group (FvL – LION). He investigates the mechanical properties of pancreatic cancer cells using a combination of high-resolution microscopy and microfabrication technologies.

The human ether-à-go-go–related gene 1 (hERG1) potassium channel is best known for its role in repolarizing excitable cells such as cardiomyocytes, but the abundance of this cardiac channel is aberrantly high in cancer cells.
We recently investigated the interaction of hERG1 with the b1 integrin subunit, a member of a family of adhesion molecules, at the plasma membrane of human cancer cells. The open and closed states of hERG1 channels (i.e. increased and reduced K+ efflux respectively) were found to modulate this interaction. In immunodeficient mice, proliferation was inhibited in breast cancer cells expressing forms of hERG1 with an impaired K+ flow (closed state), whereas metastasis of breast cancer cells was reduced when the hERG1/β1 integrin interaction was disrupted (open state). Thus, whether hERG1 promotes proliferation or metastasis in cancer cells depends on the conformation of the channel and suggests that hERG1 inhibitors that are tailored to the channel conformation could be used to prevent different aspects of tumor progression.

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