Our collaborative study on mechanisms of venetoclax resistance is now published in #Advanced #Science journal as an Early View from Advanced Portfolio. Please check LinkedIn for a more detailed explanation and gratitude to all contributors & collaborators. advanced.onlinelibrary.wiley.com/doi/10.1002/ad…
Geert Bultynck 🇺🇦
@LMCSLeuven
The aim of Lab. Molecular & Cellular Signaling is to explore and exploit Ca2+ signaling in apoptosis and autophagy in health and disease. Views are my own.
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Using IP3R KO cells expressing single IP3R isoforms, we show that anti-apoptotic BCL-2 proteins bind to and inhibit channel opening, Ca2+ signals & ER-mitochondrial Ca2+ transfers mediated by all three IP3R isoforms. So, BCL-2 is a general IP3R modulator!
Using IP3R KO cells expressing single IP3R isoforms, we show that anti-apoptotic BCL-2 proteins bind to and inhibit channel opening, Ca2+ signals & ER-mitochondrial Ca2+ transfers mediated by all three IP3R isoforms. So, BCL-2 is a general IP3R modulator!
Happy to share our @NatureComms on how ryanodine receptors control lysosomes to stay on call for autophagy or to get out of the cell for lysosomal secretion via the RyR2::ATP6v0a1 hub at ER-lysosomal contact sites! nature.com/articles/s4146…
Another important moonlighting function of V-type ATPases by impacting other organelles!
🚨 New from our lab (est. 2020) — now published in Nature Communications!View quoted post on X
🧬We uncover a surprising link between the v-ATPaseand mitochondrial function:
Mild v-ATPase inhibition restores cell fitness under mitochondrial mistranslation stress
nature.com/articles/s4146…
(Thread ⬇️)
Happy to share our most recent paper unlocking the role of the Fe-S-cluster-binding protein CISD2 underlying the health of human neurons. The key lies in its ability to sustain mitochondrial function by promoting ER-mitochondrial contact sites!
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