Reactive oxygen species trigger motoneuron death in non cell autonomous models of als through activation of c Abl signaling

The aim of this study was to determine, through a preliminary in vitro study on human glioblastoma (A172, LN229), anaplastic glioma (SF268) and neuroblastoma (SK-N-SH) cell lines,

1) Lamin A/C deficiency does not affect CD4 + T-cell development. 2) Lamin A/C participates in CD4 + T-cell activation by upregulating CD69 and CD25 through

Peripheral (intraperitoneal) co-administration of the α7 nAChR agonist PNU282987 with LPS, attenuated body weight loss and sickness behavior associated with LPS challenge in adult

Second, all age and  gender groups are statistically  significant. In comparison  with the  reference  category  (woman  over  64  years),  belonging  to 

These initial results led us to further explore the functional pathophysiological role of GPR107  in  PCa  cell  models.  The  first  approach  was  to  assess 

The formation of mitochondrial reactive oxygen and nitrogen species may lead to endothelial dysfunction by the activation of the vascular and phagocy- tic NOXs through protein kinase

fluorescent dyes) for in vivo imaging of living tissues are: i) permeation of a substrate is not required, making non-invasive techniques for in vivo monitoring of ROS/redox

Using immune synapse (IS) formation as a model of polarized vesicle trafficking, our group identified SNX27 association with the PDZ- binding diacylglycerol kinase..