Protein-RNA interactions mediated by silvestrol-insight into a unique molecular clamp.

Molecular staples or interfacial inhibitors are small molecules that exert their activity through co-association with macromolecules leading to various effects on target functions. Some molecules inhibit target activity, while others generate gain-of-function complexes. We and others have previously identified two structurally distinct classes of molecular staples, pateamine A and rocaglates.

Synthesis of polyurethanes through the oxidative decarboxylation of oxamic acids: a new gateway toward self-blown foams.

Polyurethane (PU) thermoplastics and thermosets were prepared through the step-growth polymerization of generated polyisocyanates through the decarboxylation of polyoxamic acids, in the presence of phenyliodine diacetate (PIDA), and polyols. The CO produced during the reaction allowed the access to self-blown polyurethane foams through an endogenous chemical blowing. The acetic acid released from ligand exchange at the iodine center was also shown to accelerate the polymerization reaction, avoiding the recourse to an additional catalyst.

Copper-Mediated Synthesis of N-Aryl-Oxamic Acids.

The Cu-catalyzed Ullmann-Goldberg cross-coupling between aryl iodides and oxamates is shown to afford the corresponding N-aryloxamates with yields ranging from moderate to excellent, when the oxamate precursor incorporates a bulky tertiary alkyl group effectively preventing product degradation under the strongly basic reaction conditions. The final oxamic acids are then generated through the acid hydrolysis of the oxamate in high yields. These acids were then converted into urethanes using PIDA under thermal conditions or a visible-light Fe-LMCT process.

loss in neural progenitor cells suppresses translation of ASD/NDD-associated transcripts in an mTORC1- and MNK1/2-reversible fashion.

Tuberous sclerosis complex (TSC) is an inherited neurodevelopmental disorder (NDD) with frequent manifestations of epilepsy and autism spectrum disorder (ASD). TSC is caused by inactivating mutations in or tumor suppressor genes, with encoded proteins hamartin (TSC1) and tuberin (TSC2) forming a functional complex inhibiting mechanistic target of rapamycin complex 1 (mTORC1) signaling. This has led to treatment with allosteric mTORC1 inhibitor rapamycin analogs ("rapalogs") for TSC tumors; however, rapalogs are ineffective for treating neurodevelopmental manifestations.