Chlorination-Supported Shrinkage of C60 Fullerene to Non-classical C58 Cages.

We provide important novel insights into skeletal transformations of fullerene by reporting new cases of cage shrinkage in the most abundant C60 fullerene via a C2 loss. High-temperature (400-500 oC) chlorination of IPR C60 with SbCl5 or SbCl5/SbCl3 mixtures predominantly gives non-IPR C60Cln compounds via Stone-Wales rearrangements, but the present study further reveals non-classical C58Cln chlorofullerenes as by-products. The new C58(NC1)Cl20 and C58(NC1)Cl24 chlorides have been isolated by air-free HPLC and structurally characterized by X-ray crystallography.

Phosphorylation-driven epichaperome assembly is a regulator of cellular adaptability and proliferation.

The intricate network of protein-chaperone interactions is crucial for maintaining cellular function. Recent discoveries have unveiled the existence of specialized chaperone assemblies, known as epichaperomes, which serve as scaffolding platforms that orchestrate the reconfiguration of protein-protein interaction networks, thereby enhancing cellular adaptability and proliferation. This study explores the structural and regulatory aspects of epichaperomes, with a particular focus on the role of post-translational modifications (PTMs) in their formation and function.

Combination of MDM2 and Targeted Kinase Inhibitors Results in Prolonged Tumor Control in Lung Adenocarcinomas With Oncogenic Tyrosine Kinase Drivers and Amplification.

Purpose: MDM2, a negative regulator of the TP53 tumor suppressor, is oncogenic when amplified. amplification (MDM2amp) is mutually exclusive with mutation and is seen in 6% of patients with lung adenocarcinoma (LUAD), with significant enrichment in subsets with receptor tyrosine kinase (RTK) driver alterations. Recent studies have shown synergistic activity of MDM2 and MEK inhibition in patient-derived LUAD models with MDM2amp and RTK driver alterations.