selective par 1 antagonist  (Selleck Chemicals)

Journal: Cancer Gene Therapy

Article Title: B-cell clonogenic activity of HIV-1 p17 variants is driven by PAR1-mediated EGF transactivation

doi: 10.1038/s41417-020-00246-9

Figure Lengend Snippet: Different molecules used in B-cell colony assays.

Article Snippet: SCH79797 , – , 10 nM , Selective antagonist of PAR-1 , Tocris Bioscience, Bristol, UK.

Techniques: Concentration Assay

Journal: Journal of Cerebral Blood Flow & Metabolism

Article Title: Depression following traumatic brain injury in mice is associated with down-regulation of hippocampal astrocyte glutamate transporters by thrombin

doi: 10.1177/0271678X17742792

Figure Lengend Snippet: Thrombin acts on the PAR-1 receptor to decrease the expression of GLT1 and GLAST and to cause depressive behaviors. (a) Atlas shows in vivo PAR-1AP injection site. (b–d) Representative Western blots and quantification of the effect of intraventricular (icv) administration of PAR-1 agonist peptide (AP) on levels of GLT1, GLAST, and phospho-MYPT1. Hippocampal levels of GLT1 (b), GLAST (c) phospho-MYPT1 (d) were quantified seven days following exposure to PAR-1AP (20 µM icv for 24 h) or control peptide. There was a trend toward a decrease in GLT1 and increase in phospho-MYPT1 in the PAR-1AP infused mice but this did not reach significance. The decrease in GLAST in the PAR-1 AP treated mice was significant. (e–g) Quantification of depressive-like behaviors on day 7–9 of recovery showed an increase in immobile time in the FST (E), but not TST (f) or sucrose preference (g) test (n = 10; *p < 0.05, vs. control peptide). (h–j) The PAR-1 inhibitor SCH79797 25 (mg/kg, i.p.) was administered 3 h after TBI and the expression of GLT1 and GLAST examined in the hippocampus by Western blot. (h, i) Treatment with SCH79797 attenuated the decrease in levels of GLT1 and GLAST 1 day after TBI (n = 7–8 per group; *p < 0.05 vs. sham; #p < 0.05 vs. TBI-Saline). (j) Quantification of depressive-like behavior on day 7 of recovery showed an increase in immobile time in saline-treated TBI mice in the TST. Immobile time in mice treated with SCH79797 following TBI was not significantly different from sham controls. (n = 7–9 per group; *p < 0.05 vs. sham). AP, PAR-1 agonist peptide.

Article Snippet: Based on our in vitro results and published work, 36 20 μM peptides were infused for 24 h. Other drug administration The selective PAR-1 antagonist SCH79797 (25 μg/kg; Tocris) was administered via intraperitoneal (IP) injection 3 h after TBI.

Techniques: Expressing, In Vivo, Injection, Western Blot, Control, Saline