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van Berkum, E.

Publications and source records attributed to van Berkum, E..

2 recordsLinked to original sources

A cell-based degrader assessment platform facilitates discovery of functional NUDT5 PROTACs

Targeted protein degradation (TPD) via PROTACs and molecular glues holds significant therapeutic promise but demands detailed mechanistic evaluation in live cells to fully understand compound behavior and optimize efficacy. Here, we present an integrated, cell-first platform that combines a modular degradation assay with E3 ligase target engagement readouts for comprehensive assessment of TPD molecules in cells and use it to evaluate PROTACs towards NUDT5. To mimic endogenous degradation conditions and TPD amenability, we established a fusion protein expression system consisting of a lysine-free FKBP12 F36V PROTAC handle (FKBPVK0) and used a HiBiT/akaLuc dual luciferase reporter to accurately measure degradation dynamics. This set-up identified a VHL-dependent NUDT5 PROTAC, DDD2, that induced robust NUDT5 degradation, despite impaired NUDT5 binding in vitro and in cellulo, but no CRBN-dependent degraders. NUDT5 lysine availability mapping with DDD2 and FKBP12 F36V-directed PROTACs suggested that the CRL4CRBN complex is more sensitive to target lysine accessibility than CRL2VHL, which may have implications for E3 ligase choice and therapeutic resistance. CeTEAM drug biosensors were also established towards CRBN and VHL to quantitatively monitor degrader engagement in living cells and confirmed that the tested CRBN-directed NUDT5 PROTACs poorly engaged the E3. All together, this platform provides a versatile and scalable framework for TPD molecule discovery in a cellular context.

biochemistry↗

Aurora B controls microtubule stability to regulate abscission dynamics in stem cells

Abscission is the last step of cell division leading to the complete separation of the two sister cells and consists of the cutting of a cytoplasmic bridge. Abscission is mediated by the ESCRT membrane remodeling machinery which also triggers the severing of a thick bundle of microtubules that needs to be cleared prior to abscission. Here, we show that rather than being passive actors in abscission, microtubules control abscission speed. Using mouse embryonic stem cells, which transition from slow to fast abscission during exit from naive pluripotency, we investigate the molecular mechanism for the regulation of abscission dynamics and identify a feedback loop between the activity of Aurora B and microtubule stability. We demonstrate that naive stem cells maintain high Aurora B activity after cytokinesis. This high Aurora B activity leads to transient microtubule stabilization that delays abscission. In turn, stable microtubules promote the activity of Aurora B. When cells exit naive pluripotency, a decrease in Wnt signaling leads to a decrease in the activity of Aurora B, less stable microtubules, and a faster abscission. Overall, our data demonstrate that Aurora B-dependent microtubule stability controls abscission dynamics.

cell biology↗