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In our model, the absence of TrkB signalling in iSPN + led to specific upregulation of Gsto2 at the pre-symptomatic stage, followed by a sharp decrease to baseline levels by 8 months (Fig

Mechanistically, we find that catechol estrogens elicit their neuroprotection in HT22 cells by directly targeting PDI and subsequently inhibiting PDI-mediated conversion of nNOS and iNOS monomers to the catalytically-active homodimers, and ultimately, prevents chemically-induced ferroptosis

Facile installation of post-translational modifications on the tau protein via chemical mutagenesis

Farfariello, V

The effect of homocysteine on the clinical outcomes of ventilated patients with severe sepsis

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