Topic: AKT

1-Methyl-4-phenyl-pyridinium (MPP+) and 6-hydroxydopamine (6-OHDA) are the predominant neurotoxic agents used in the research of Parkinson's disease (PD). The mTORC2 is a significant signaling pathway whose specific functions and mechanisms remain partially elusive, especially in the context of PD-related oxidative stress. We aimed to determine the interconnection between mTORC2 and oxidative stress in MPP+ and 6-OHDA neurotoxic models of PD. All experiments were performed on the human neuroblastoma cell line, SH-SY5Y. Cells were divided into two groups: control (consists of control cells and

Mutations in Na+/H+ exchanger NHE6 (SLC9A6) underlie several X-linked developmental brain disorders including the neurodegenerative disease Christianson Syndrome (CS). Symptoms include cerebellar atrophy, non-verbal status, seizures and severe cognitive disabilities. NHE6 deletion or loss-of-function mutations lead to attenuated endosomal signaling, dysregulated synaptic transmission and abnormal dendritic branching in vitro and in vivo [1]. In this project, we aim to investigate the localization of wildtype- and CS-associated NHE6 variants in primary neurons, the importance of NHE6 in recepto

We recently identified Protein kinase N1 (PKN1) as a negative regulator of neuronal AKT activity during postnatal cerebral development. Given the pivotal role of the AKT pro-survival signalling cascade in ischemia/reperfusion, our investigation aimed to determine whether PKN1-mediated AKT inhibition remains relevant during pathological conditions in the mature brain. Employing adult wild type and global Pkn1 knockout (Pkn1-/-) mice, we observed that Pkn1 knockout indeed imparts a protective phenotype in both, in vitro and in vivo stroke models. However, this was not associated with enhanced AK

Endocrine disruptors (EDs) are ubiquitous compounds with the ability to interfere with endogenous hormones. Molecules identified as EDs are highly heterogeneous, but most of them are man-made chemicals, such as ethinyl estradiol (EE), medication, perfluorooctanesulfonic-acid (PFOS), surfactant, and diethyl-phthalate (DP), plasticizer. The constant exposure of the global population to these molecules can lead to an induction of toxic effects, especially on the central nervous system. Among the different mechanisms by which EDs could influence human health, of interest is the modulation of micro