Positive regulation of the CREB phosphorylation via JNK-dependent pathway prevents antimony-induced neuronal apoptosis in PC12 cell and mice brain.

Antimony (Sb) is a potentially toxic chemical element abundantly found in the environment. We previously reported that Sb promoted neuronal deathvia reactive oxygen species-dependent autophagy. Here, we assessed the role of cyclic adenosine monophosphate response element-binding protein (CREB) in Sb-induced neuronal damage.

PKA- and Ca-dependent p38 MAPK/CREB activation protects against manganese-mediated neuronal apoptosis.

Although manganese (Mn) is an essential trace element, its excessive consumption may lead to neuronal death and neurodegenerative disorders. Human cells launch adaptive responses to attenuate Mn-induced neurotoxicity. However, the regulation of the responsive proteins and their function during Mn-stimulated neurotoxicity remain largely unknown.

SIRT1 downregulation mediated Manganese-induced neuronal apoptosis through activation of FOXO3a-Bim/PUMA axis.

Manganese (Mn) is an essential trace element. Excessive exposure to Mn may lead to neuronal death and neurodegenerative disorders. Accumulating evidence has shown that silent mating type information regulation 2 homolog 1 (SIRT1) plays a vital role in brain damage.