Discovery of a Trifluoromethoxy Cyclopentanone Benzothiazole Receptor-Interacting Protein Kinase 1 Inhibitor as the Treatment for Alzheimer’s Disease by Yi Sun (118759)

“…<b>SZM679</b>, a highly specific RIPK1 inhibitor (<i>K</i>_d,RIPK1 = 8.6 nM, <i>K</i>_d,RIPK3 > 5000 nM), was developed by our group with superior high antinecroptotic activity (EC₅₀ = 2 nM), and investigated to completely reverse the tumor necrosis factor-induced systemic inflammatory response syndrome. …”

Discovery of a Trifluoromethoxy Cyclopentanone Benzothiazole Receptor-Interacting Protein Kinase 1 Inhibitor as the Treatment for Alzheimer’s Disease by Yi Sun (118759)

“…<b>SZM679</b>, a highly specific RIPK1 inhibitor (<i>K</i>_d,RIPK1 = 8.6 nM, <i>K</i>_d,RIPK3 > 5000 nM), was developed by our group with superior high antinecroptotic activity (EC₅₀ = 2 nM), and investigated to completely reverse the tumor necrosis factor-induced systemic inflammatory response syndrome. …”

Discovery of a Trifluoromethoxy Cyclopentanone Benzothiazole Receptor-Interacting Protein Kinase 1 Inhibitor as the Treatment for Alzheimer’s Disease by Yi Sun (118759)

“…<b>SZM679</b>, a highly specific RIPK1 inhibitor (<i>K</i>_d,RIPK1 = 8.6 nM, <i>K</i>_d,RIPK3 > 5000 nM), was developed by our group with superior high antinecroptotic activity (EC₅₀ = 2 nM), and investigated to completely reverse the tumor necrosis factor-induced systemic inflammatory response syndrome. …”

Discovery of a Trifluoromethoxy Cyclopentanone Benzothiazole Receptor-Interacting Protein Kinase 1 Inhibitor as the Treatment for Alzheimer’s Disease by Yi Sun (118759)

“…<b>SZM679</b>, a highly specific RIPK1 inhibitor (<i>K</i>_d,RIPK1 = 8.6 nM, <i>K</i>_d,RIPK3 > 5000 nM), was developed by our group with superior high antinecroptotic activity (EC₅₀ = 2 nM), and investigated to completely reverse the tumor necrosis factor-induced systemic inflammatory response syndrome. …”

Discovery of a Trifluoromethoxy Cyclopentanone Benzothiazole Receptor-Interacting Protein Kinase 1 Inhibitor as the Treatment for Alzheimer’s Disease by Yi Sun (118759)

“…<b>SZM679</b>, a highly specific RIPK1 inhibitor (<i>K</i>_d,RIPK1 = 8.6 nM, <i>K</i>_d,RIPK3 > 5000 nM), was developed by our group with superior high antinecroptotic activity (EC₅₀ = 2 nM), and investigated to completely reverse the tumor necrosis factor-induced systemic inflammatory response syndrome. …”

CRIF1 deletion stimulated the activation of the NF-κB signaling pathway in HUVECs. by Shuyu Piao (4731327)

Change in per capita growth rate of intraspecies cooperating population implemented with a continuous model. by Yaron Goldberg (10164674)

Fig 2 - by Masaru Sakai (1669627)

SIRT1 mediated CRIF1 deficiency-induced NF-κB activation in HUVECs. by Shuyu Piao (4731327)

Absence of Jag2 alleviates hypoxia-induced oxidative stress injury in rats. by Hanhan Liu (568151)

PAM16 correlation with N-MYC. by Zahra Motahari (6814013)

Expression of MAGMAS in medulloblastoma. by Zahra Motahari (6814013)

MAGMAS inhibition on mitochondrial activity in medulloblastoma cells. by Zahra Motahari (6814013)

Inhibition of Jag2 effectively ameliorates hypoxia-induced PH in rats. by Hanhan Liu (568151)

Jag2 expression is upregulated in hypoxia-treated rats and PASMCs. by Hanhan Liu (568151)

MAGMAS inhibition induces medulloblastoma cell death. by Zahra Motahari (6814013)

BT9 reduces DAOY and D425 medulloblastoma cell invasion. by Zahra Motahari (6814013)

The effect of MAGMAS inhibition on mitochondrial respiration and acidification rate in D425 cells. by Zahra Motahari (6814013)

MAGMAS inhibition reduces DAOY cells migration. by Zahra Motahari (6814013)

Nitric Oxide Oxidatively Nitrosylates Ni(I) and Cu(I) <i>C</i>-Organonitroso Adducts by Stefan Wiese (1626535)

“…[Me₂NN]Cu(NCMe) reacts with 0.5 equiv of ArNO in ether to give the dinuclear adducts {[Me₂NN]Cu}₂(μ-η²:η¹-ONAr) (<b>2a</b> and <b>2b</b>), which exhibit η² and η¹ bonding of the ArNO moiety with separate [Me₂NN]Cu fragments possessing N−O distances of 1.375(6) Å (<b>2a</b>) and 1.368(2) Å (<b>2b</b>). …”