Deshydroxy LY-411575 has been used in dibenzazepine (DBZ) treatment[1] and chemical treatment.[2]
Biochem/physiol Actions
Deshydroxy LY-411575 is a cell-permeable γ-secretase inhibitor and inhibtor of Notch processing.
Deshydroxy LY-411575 is a cell-permeable γ-secretase inhibitor and inhibtor of Notch processing. Deshydroxy LY-411575 significantly lowers both brain and plasma Aβ40 levels by ~72% in Tg2576 mutant APP transgenic mouse model and potently blocks Notch processing, with an IC50 of 1.7 nM in SupT1 cells.
LY411575 prevents SPP (signal peptide peptidase) dependent cleavage of HCV (hepatitis C virus) core protein.[3]
During development, hematopoietic stem cells (HSCs) undergo a rapid expansion in the fetal liver (FL) after their emergence in the aorta-gonad-mesonephros (AGM) region. We recently reported that the endolysosomal trafficking factor BLOS2, encoded by the Bloc1s2 gene, regulates HSC/hematopoietic progenitor
Inhibitory effect of presenilin inhibitor LY411575 on maturation of hepatitis C virus core protein, production of the viral particle and expression of host proteins involved in pathogenicity.
Otoguro T, et al.
Microbiology and Immunology, 60(11), 740-753 (2016)
Development (Cambridge, England), 149(10) (2022-05-04)
The earliest hematopoietic stem and progenitor cells (HSPCs) are generated from the ventral wall of the dorsal aorta, through endothelial-to-hematopoietic transition during vertebrate embryogenesis. Notch signaling is crucial for HSPC generation across vertebrates; however, the precise control of Notch during
G protein-coupled receptor 183 facilitates endothelial-to-hematopoietic transition via Notch1 inhibition.
Expansion of pulmonary neuroendocrine cells (PNECs) is a pathological feature of many human lung diseases. Human PNECs are inherently difficult to study due to their rarity (<1% of total lung cells) and a lack of established protocols for their isolation.
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