Photoinduced Charge Transfer Empowers TaC and NbC MXenes with High SERS Performance.

This study introduces two-dimensional (2D) TaC and NbC MXenes as outstanding materials for surface-enhanced Raman scattering (SERS) sensing, marking a significant departure from traditional noble-metal substrates. These MXenes exhibit exceptional SERS capabilities, achieving enhancement factors around 10 and detection limits as low as 10 M for various analytes, including environmental pollutants and drugs. The core of their SERS functionality is attributed to the robust interfacial photoinduced charge-transfer interactions between the MXenes and the adsorbed molecules.

Charge-transfer-driven ultrasensitive SERS sensing in a two-dimensional titanium carbonitride MXene.

Two-dimensional (2D) MXenes stand out as promising platforms for surface-enhanced Raman scattering (SERS) sensing owing to their metallic feature, various compositions, high surface area, compatibility with functionalization, and ease of fabrication. In this work, we report a high-performance 2D titanium carbonitride (TiCN) MXene SERS substrate. We reveal that the abundant electronic density of states near the Fermi level of TiCN MXene boosts the efficiency of photo-induced charge transfer at the interface of TiCN/molecule, resulting in significant Raman enhancement.

Two-dimensional MBenes with ordered metal vacancies for surface-enhanced Raman scattering.

As an emerging class of two-dimensional (2D) materials, MBenes show enormous potential for optoelectronic applications. However, their use in molecular sensing as surface-enhanced Raman scattering (SERS)-active material is unknown. Herein, for the first time, we develop a brand-new high-performance MBene SERS platform.

Smoothened is a therapeutic target for reducing glutamate toxicity in ischemic stroke.

Extracellular glutamate contributes to brain damage in ischemia. Under physiological conditions, glutamate transporters are responsible for regulating its intracellular/extracellular concentrations in the brain. However, how the extracellular glutamate is regulated in ischemia remains unclear.

Robo functions as an attractive cue for glial migration through SYG-1/Neph.

As one of the most-studied receptors, Robo plays functions in many biological processes, and its functions highly depend on Slit, the ligand of Robo. Here we uncover a Slit-independent role of Robo in glial migration and show that neurons can release an extracellular fragment of Robo upon cleavage to attract glia during migration in . Furthermore, we identified the conserved cell adhesion molecule SYG-1/Neph as a receptor for the cleaved extracellular Robo fragment to mediate glial migration and SYG-1/Neph functions through regulation of the WAVE complex.

Sonic hedgehog induces GLT-1 degradation via PKC delta to suppress its transporter activities.

GLT-1 is mainly expressed in astrocytes and has a crucial role in glutamate uptake. Sonic hedgehog (SHH) can inhibit glutamate uptake and its pathway is activated in many brain diseases related with glutamate excitotoxicity. However, whether SHH regulates GLT-1 to affect glutamate uptake is not clear.

TRPC6 expression in neurons is differentially regulated by NR2A- and NR2B-containing NMDA receptors.

The expression of transient receptor potential canonical 6 (TRPC6) in central nervous system (CNS) is important for neuronal functions and certain neural disorders. However, the regulatory mechanism of TRPC6 expression in neurons is still obscure. In this study, we show that TRPC6 expression in the primary cultured cortical neurons is bidirectionally regulated by glutamate.

RIP3 S-nitrosylation contributes to cerebral ischemic neuronal injury.

Cerebral ischemia-reperfusion is associated with NMDA receptor-mediated calcium influx which activates neuronal nitric oxide synthase (nNOS) and consequently induces NO production. NO S-nitrosylates cellular protein and aggravates neuronal injury. Receptor-interacting protein 3 (RIP3) is a sensor molecule regulating cell apoptosis and necrosis.

N-methyl-D-aspartate receptor-dependent denitrosylation of neuronal nitric oxide synthase increase the enzyme activity.

Our laboratory once reported that neuronal nitric oxide synthase (nNOS) S-nitrosylation was decreased in rat hippocampus during cerebral ischemia-reperfusion, but the underlying mechanism was unclear. In this study, we show that nNOS activity is dynamically regulated by S-nitrosylation. We found that overexpressed nNOS in HEK293 (human embryonic kidney) cells could be S-nitrosylated by exogenous NO donor GSNO and which is associated with the enzyme activity decrease.