Reversal of regioselectivity in reactions of donor-acceptor cyclopropanes with electrophilic olefins.

Reactivity of donor-acceptor cyclopropanes towards nucleophiles and electrophiles is determined by the specific philicity of the carbon atoms originating from the strong polarization of the central C-C bond. Herein, we report that vitamin B catalysis enables the transformation of an initially electrophilic center into a nucleophilic radical that reacts with SOMOphiles. This radical-based strategy reverses the standard regioselectivity and thus complements the classical approaches.

Strain release - an old tool for new transformations.

Strain-release driven transformations give access to attractive bioisosteric motifs highly prized by medicinal chemists and they are characteristic of molecules possessing distorted bond lengths and angles. By broadening the chemical space in drug discovery, recently, these compounds have attracted a lot of interest. Their reactivity stems mainly from an increased energy and destabilization.

Polarity-Reversal Strategy for the Functionalization of Electrophilic Strained Molecules via Light-Driven Cobalt Catalysis.

Strain-release-driven methodology is a powerful tool for accessing structural motifs, highly desirable by the pharmaceutical industry. The reactivity of spring-loaded cyclic reagents is dominated by transformations relying on their inherent electrophilic reactivity. Herein, we present a polarity-reversal strategy based on light-driven cobalt catalysis, which enables the generation of nucleophilic radicals through strain release.

Photoinduced Vitamin B-Catalysis for Deprotection of (Allyloxy)arenes.

Vitamin B is a natural cobalt complex that, while reduced to the "supernucleophilic" Co(I) form, can easily react with electrophiles via an S2 mechanism. It is also shown to react via an S2' mechanism with allylic compounds allowing for photochemical deprotection of (allyloxy)arenes. A sustainable alternative to commonly used noble metal-catalyzed deprotection reactions is presented.

Dynamic JUNQ inclusion bodies are asymmetrically inherited in mammalian cell lines through the asymmetric partitioning of vimentin.

Aging is associated with the accumulation of several types of damage: in particular, damage to the proteome. Recent work points to a conserved replicative rejuvenation mechanism that works by preventing the inheritance of damaged and misfolded proteins by specific cells during division. Asymmetric inheritance of misfolded and aggregated proteins has been shown in bacteria and yeast, but relatively little evidence exists for a similar mechanism in mammalian cells.