Publications by authors named "J Nathan"
Article Synopsis
- Glioblastoma (GBM) is the deadliest brain tumor in adults, and current therapies are largely ineffective, which drives the need for new treatment strategies based on the tumor's metabolic needs, specifically glucose and glutamine.
- A ketogenic metabolic therapy (KMT) approach targets these metabolic pathways by combining dietary changes with specific drugs to limit glycolysis and glutaminolysis, while promoting the use of non-fermentable fuels like ketones and fatty acids.
- The glucose-ketone index (GKI) serves as a biomarker to monitor treatment effectiveness, aiming to create a more hostile environment for tumor growth and improve outcomes in GBM as well as potentially other cancer types reliant on similar metabolic pathways.
A closer look at the role of deubiquitinating enzymes in the Hypoxia Inducible Factor pathway.
Biochem Soc Trans
December 2024
Article Synopsis
- - HIFs are key regulators that help cells adapt to low oxygen levels (hypoxia), but they are degraded in normal oxygen conditions through a process involving the VHL E3 ligase and ubiquitination.
- - The review examines the complex interactions between ubiquitination and deubiquitination enzymes (DUBs) in regulating HIF signaling under different oxygen levels, highlighting the significance of DUBs in modulating the effects of VHL.
- - It also explores the dual roles of DUBs in hypoxia, both in systems that rely on VHL and those that don't, while discussing the potential therapeutic implications of inhibiting these enzymes.
Clear cell renal cell carcinoma (ccRCC) represents the most common form of kidney cancer and is typified by biallelic inactivation of the von Hippel-Lindau () tumour suppressor gene. Here, we undertake genome-wide CRISPR/Cas9 screening to reveal synthetic lethal interactors of , and uncover that loss of Core Binding Factor β (CBF-β) causes cell death in -null ccRCC cell lines and impairs tumour establishment and growth . This synthetic relationship is independent of the elevated activity of hypoxia inducible factors (HIFs) in -null cells, but does involve the RUNX transcription factors that are known binding partners of CBF-β.
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