New insights into carbon-based and MXene anodes for Na and K-ion storage: A review

Na-ion batteries and K-ion batteries are promising alternatives to vastly used lithium-ion batteries mainly due to the larger natural abundance of sodium and potassium resources. Carbon-based and MXene materials have received increasing attention due to their unique layered structure to accommodate the larger sodium and potassium ions. It’s proposed that ionic size disparity (K^(+): 1.38 Å;Na^(+): 0.97 Å;Li^(+): 0.76 Å) leads to sluggish intercalation and extraction kinetics in larger alkali metal ions (AMIs). Nevertheless, the electrochemical inactivity of sodium intercalation in graphite suggests that different chemical properties of AMs and their interactions with carbon host and electrolytes is crucial for interfacial instability and irreversible capacity loss. Structural modifications by expanding interlayer spacing and defect engineering enable reduced diffusion barriers and enhanced insertion of sodium or potassium, but it blurs the electrochemical performance between battery and capacitor. This review provides insight into 2D carbon materials and their architectures for Na and K-ion batteries through an in-depth analysis of structure–property interdependence and different electrochemical mechanisms supported by both experimental and theoretical data to discuss the promises and challenges of post-lithium batteries. Finally, the perspectives and potential directions regarding material design concepts for 2D carbon-based nanomaterials and MXene phases for metal-ion storage are proposed.

Cbl negatively regulates JNK activation and cell death

Here, we explore the role of Cbl proteins in regulation of neuronal apoptosis. In two paradigms of neuron apoptosis -- nerve growth factor （NGF） deprivation and DNA damage -- cellular levels of c-Cbl and Cbl-b fell well before the onset of cell death. NGF deprivation also induced rapid loss of tyrosine phosphorylation （and most likely, activation） of c-Cbl. Targeting c-Cbl and Cbl-b with siRNAs to mimic their loss/inactivation sensitized neuronal cells to death promoted by NGF deprivation or DNA damage. One potential mechanism by which Cbl proteins might affect neuronal death is by regulation of apoptotic c-Jun N-terminal kinase （JNK） signaling. We demonstrate that Cbl proteins interact with the JNK pathway components mixed lineage kinase （MLK） 3 and POSH and that knockdown of Cbl proteins is sufficient to increase JNK pathway activity. Furthermore, expression of c-Cbl blocks the ability of MLKs to signal to downstream components of the kinase cascade leading to JNK activation and protects neuronal cells from death induced by MLKs, but not from downstream JNK activators. On the basis of these findings, we propose that Cbls suppress cell death in healthy neurons at least in part by inhibiting the ability of MLKs to activate JNK signaling. Apoptotic stimuli lead to loss of Cbl protein/activity, thereby removing a critical brake on JNK activation and on cell death.