WebJun 25, 2024 · We identify TRIM37 as a key mediator of growth arrest when PLK4 activity is partially or fully inhibited but is not required for growth arrest triggered by supernumerary centrosomes. Moreover, this activity is independent of its role as an E3 ligase and distinct from other TRIM37 functions described to date. WebTRIM37 controls cancer-specific vulnerability to PLK4 inhibition. Targeting TRIM37-driven centrosome dysfunction in 17q23-amplified breast cancer. TRIM37 has a role in …
Targeting TRIM37-driven centrosome dysfunction in 17q23 …
WebApr 11, 2024 · The ubiquitin ligase TRIM37 localizes to centrosomes, but its centrosomal roles are not yet defined. ... In Xenopus extracts, PLK4 … WebJun 27, 2024 · TRIM37 interacts with PLK4 and CEP192 ( Meitinger et al., 2024 ). Although TRIM37 can promote ubiquitination of PLK4, it is distinct from SCF β−TRCP modification since it does not result in changes to PLK4 abundance ( Meitinger et al., 2024 ). cornerstone way reno nv
Targeting TRIM37-driven centrosome dysfunction in 17q23-amplified ...
WebJul 1, 2024 · TRIM37 deletion restored the ability of cells to proliferate in centrinone. Thus, centrosome removal via Plk4 inhibition appears to be a promising strategy for … WebAug 5, 2024 · TRIM37 amplification has been observed in a large number of cancers, and synthetic lethality of PLK4 inhibitors in TRIM37-amplified breast cancer, which accounts for approximately 10% of breast cancers, has been confirmed [18, 19]. Therefore, inhibition of PLK4 using PLK4 small-molecule inhibitors provides a new approach to trigger selective ... WebSep 18, 2024 · When TRIM37 is more active, centrosomes do not behave correctly and errors occur during cell division, leading to the overactive cell division that results in tumors. 1 An enzyme called PLK4 kickstarts the errant cell division process in … fanshawe operations management