Correction: Temporal control of protein labeling by a photo-caged benzaldehyde motif and discovery of host cell factors of avian influenza virus infection.

Correction for 'Temporal control of protein labeling by a photo-caged benzaldehyde motif and discovery of host cell factors of avian influenza virus infection' by Nicholas Asiimwe et al., Chem. Commun., 2022, https://doi.org/10.1039/d2cc04091c.

Temporal control of protein labeling by a photo-caged benzaldehyde motif and discovery of host cell factors of avian influenza virus infection.

Photo-caged benzaldehyde probes using o-nitrophenylethylene glycol were designed for photo-activated electrophile generation. Using photo-activated electrophile generating probes, we successfully revealed under-represented host cell response factors using an avian influenza virus infection model.

The discovery of penta-peptides inhibiting the activity of the formylglycine-generating enzyme and their potential antibacterial effects against Mycobacterium tuberculosis.

The formylglycine-generating enzyme is a key regulator that converts sulfatase into an active form. Despite its key role in many diseases, enzyme activity inhibitors have not yet been reported. In this study, we investigated penta-peptide ligands for FGE activity inhibition and discovered two hit peptides. In addition, the lead peptides also showed potential antibacterial effects in a Mycobacterium tuberculosis model.

Photoactivatable metabolic warheads enable precise and safe ablation of target cells in vivo.

Photoactivatable molecules enable ablation of malignant cells under the control of light, yet current agents can be ineffective at early stages of disease when target cells are similar to healthy surrounding tissues. In this work, we describe a chemical platform based on amino-substituted benzoselenadiazoles to build photoactivatable probes that mimic native metabolites as indicators of disease onset and progression. Through a series of synthetic derivatives, we have identified the key chemical groups in the benzoselenadiazole scaffold responsible for its photodynamic activity, and subsequently designed photosensitive metabolic warheads to target cells associated with various diseases, including bacterial infections and cancer. We demonstrate that versatile benzoselenadiazole metabolites can selectively kill pathogenic cells - but not healthy cells - with high precision after exposure to non-toxic visible light, reducing any potential side effects in vivo. This chemical platform provides powerful tools to exploit cellular metabolic signatures for safer therapeutic and surgical approaches.

Nitric Oxide: Exploring the Contextual Link with Alzheimer's Disease.

Neuronal inflammation is a systematically organized physiological step often triggered to counteract an invading pathogen or to rid the body of damaged and/or dead cellular debris. At the crux of this inflammatory response is the deployment of nonneuronal cells: microglia, astrocytes, and blood-derived macrophages. Glial cells secrete a host of bioactive molecules, which include proinflammatory factors and nitric oxide (NO). From immunomodulation to neuromodulation, NO is a renowned modulator of vast physiological systems. It essentially mediates these physiological effects by interacting with cyclic GMP (cGMP) leading to the regulation of intracellular calcium ions. NO regulates the release of proinflammatory molecules, interacts with ROS leading to the formation of reactive nitrogen species (RNS), and targets vital organelles such as mitochondria, ultimately causing cellular death, a hallmark of many neurodegenerative diseases. AD is an enervating neurodegenerative disorder with an obscure etiology. Because of accumulating experimental data continually highlighting the role of NO in neuroinflammation and AD progression, we explore the most recent data to highlight in detail newly investigated molecular mechanisms in which NO becomes relevant in neuronal inflammation and oxidative stress-associated neurodegeneration in the CNS as well as lay down up-to-date knowledge regarding therapeutic approaches targeting NO.