AKT phosphorylation

Spinal Muscular Atrophy (SMA) is a genetic disorder resulting from the deletion or mutation of the SMN1 gene (Survival Motor Neuron 1). The reduction in SMN protein levels leads to the degeneration of motor neurons in the spinal cord, giving rise to typical clinical manifestations of the disease, such as muscular weakness and atrophy. At the cellular level, SMN is part of a macromolecular machinery referred to the SMN complex, comprising various proteins, including Gemin3. Among other functions, Gemin3 regulates the intracellular survival signaling pathway NF-κB. In the context of SMA disease,

In this study, we aimed to explore methylcobalamin (MeCbl), a common treatment for peripheral nerve injuries, and its impact on macrophage phenotypes (inflammatory or anti-inflammatory) at nerve injury sites and the underlying mechanism. Using a sciatic nerve crush injury model in 6-week-old Wistar rats, we administered either saline (control group) or MeCbl (MeCbl group) via osmotic pumps for sustained systemic delivery. We assessed macrophage phenotypes in transverse sections of the sciatic nerve up to 14 days post-surgery using fluorescence immunostaining. In vitro, we induced inflammatory

…and while mTORC1 is regulated by AKT, mTORC2 is upstream of this enzyme and regulates phosphorylation of its serine 473 residue. Ribosomal protein S6 (RpS6)

Neurotoxins are numerous groups of drugs that lead detrimental effects on the neuronal system and caused the cognitive and neurological impairments. Intracellular signaling and homeostasis can disturb by those toxins. Lysosomes are crucial organelles to digest waste disposal and supply the essential materials. It is still unknown to connection between lysosomal homeostasis and neurological dysfunction. Here, we investigated how to attenuate the neurodegeneration though managing lysosomal function. After treatment of hydroperoxide as known as one of the neurotoxins, N2A cell proliferation decre

Dysregulation of synaptic plasticity was associated with numerous neurological disorders, including ischemic long-term potentiation (iLTP). Direct current stimulation (DCS) changes neuronal plasticity by the weak direct current which induces depolarization and hyperpolarization of resting membrane potential with opposite direction of polarity. FK506-binding protein 51 (FKBP51) is considered an important molecular pathway that modulates synaptic plasticity in such disease models. The correlation of the regulatory effects in plasticity under pathological condition facilitated by DCS and FKBP51 r