Massive congrats to @MallSid – just published in @NatureGenet Our study defines a series of pathway-derived subtypes (PDS), which we use as the basis for identifying a previously overlooked phenotypic landscape in colorectal cancer… https://t.co/JUE5IJqVtx 🧵👇

Great to see this out! Congrats @EsmeeVringer @HeiligRosalie @cat5863 @MitosRUs and everyone else - glad I could be a part of it! https://t.co/ddoPSUxtsL

First visualization of super-resolved GSDMD pores at the plasma membrane of pyroptotic cells!!! Fantastic work by Shirin @viten_skap and great collaboration with @PiehlerLab iBiOs Osnabrück and @HummerLab Check our preprint! https://t.co/ixW7Se5JAT

Do cells care if their mitochondrial DNA is broken? Yes! Excited to share my PhD work showing that a fraction of cells with breaks in their mtDNA recover healthy mitochondria using the integrated stress response.

Great to see this out - glad to have been part of this amazing effort. Congrats to everyone involved!

Happy to have contributed to this work by super-talented @BingxuL and @beccajcarlson. The mistery of how STING induces autophagy and NLRP3 activation is finally solved. Landmark study for the field! Human STING is a proton channel | Science

Who needs something to read these holidays??? Here a link to our new review about BCL2 family matters… https://t.co/axJcYJ93xN @CRC_1218 @Ferroptosis2306 @CECAD_ @sfb_1403 @SpringerNature

🚨🚨🚨New review from the Cancer Cell Death team, with @BertolinGiulia2 @crcl! 🚨🚨🚨 All you need to know about visualising and quantifying MOMP and mito membrane potential- Past and Future! https://t.co/61aip0oaOl

This project is part of a @FWF_at research group at @imed_tweets, with close collaboration between us, @LabiLab5, @Francesca_Fin_ and @villunger

🚨 We’re hiring! 🚨 We are looking for a motivated PhD student to come work on our exciting project trying to understand the early stages of B cell cancer development. If 🧫🧬🔬 (and ⛷️⛰️) excites you, this could be the project for you! DM or email for more info - please RT!

A new episode of „Death in the Alps“ is coming. All about cell death signalling in health and disease. Book 07-11th of January 2024 in your calendar and express your interest by emailing to deathinthealps@gmail.com so we can keep you posted! Please RT

Exciting times ahead! 🎉

Overjoyed to see my PhD paper finally out in @cddpress! #braintumour #apoptosis #neurooncology A big thank you to everyone involved and especially @MitosRus for the support and mentoring along the way. For everyone who is interested in what we found out a short summary below:

You can read the entire story for yourself, just published in @Dev_Cell

Tl;dr… Sub-lethal apoptotic stress causes oncogenic DNA damage through mitochondrial dysfunction. This dysfunction causes permeabilisation of some mitos via fission and BAX accumulation.

Also, this mechanism might help us reduce cancer treatment resistance in the future.

When might this be relevant physiologically? One possible scenario: bacteria (eg. Salmonella and Chlamydia) have been shown to cause minority MOMP, and late-stage infection is characterised by mito fragmentation, providing an ideal setting for minority MOMP-induced inflammation.

Overall, this suggests that mitochondrial dysfunction, which itself is a consequence of defective mitochondrial dynamics, promotes BAX accumulation, facilitating minority MOMP.

Not only that, but cells with hyper-fragmented mitos have more dysfunctional mitos, and these cells also maintain BAX on their mitos for longer than control cells.

We thought that dysfunctional mitos might maintain BAX on their outer membrane for a longer time than healthy mitos, which would explain why they are more sensitive to MOMP. Using imaging, we were able to test this and show that dysfunctional mitos accumulate more BAX.