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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

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

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

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