| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 200mg | 电议 |
Cell lines | PC12D Cells |
Preparation Method | PC12D cells were cultured in test medium containing 30 μM H-89 2HCl for 1 h and then exposed to fresh medium that contained both 10 pM forskolin and 30 μM H-89 2HCl. |
Reaction Conditions | 30 μM H-89 2HCl for 1h |
Applications | H-89 2HCl (30μM) significantly inhibited camp-dependent phosphorylation of histone IIh and forskolin-induced neurite outgrowth in PC12D cells. |
Animal models | Male albino mice weighing 20-25 g |
Preparation Method | H-89 2HCl (0.05, 0.1, 0.2 mg/100g) were administered intraperitoneally, 30 min before intravenous infusion of PTZ |
Dosage form | 0.05, 0.1, 0.2 mg/100g H-89 |
Applications | Intraperitoneal administration of H-89 2HCl (0.2 mg/100g) significantly increased seizure latency and threshold in PTZ-treated animals. H-89 2HCl (0.05, 0.2 mg/100g) prevented the epileptogenic activity of bucladesine (300 nM) with significant increase of seizure latency and seizure threshold. |
| 产品描述 | H-89 2HCl is A potent and selective camp-dependent protein kinase A inhibitor with IC50value of 48 nM, showing weak inhibition of PKG,PKC,Casein kinase and other kinases[1]. H-89 2HCl causes different modifications in protein phosphorylation, all of which have potential regulatory relationships with cAMP/PKA[2]. H-89 2HCl (30μM) significantly inhibited camp-dependent phosphorylation of histone IIh and forskolin-induced neurite outgrowth in PC12D cells[1]. H-89 2HCl (1-2 μM) significantly slows the repriming rate in rat skinned fibres, most likely due to it deleteriously affecting the T-system potential. H-89 2HCl (10-100 μM) inhibits net Ca2+ uptake by the SR and affectes the Ca32-sensitivity of the contractile apparatus in rat skinned fibres[4]. The PKA inhibitor H-89 2HCl effectively inhibited the CM-or PTHRP-mediated increase in UCP1 protein levels and phosphorylation of PKA substrate in ccRCC cells[6]. Trehalase (Treh) hydrolyzes trehalose to generate glucose. Pheromone biosynthesis activating neuropeptide (PBAN) treatment triggered HaTreh1 and HaTreh2 activities in the isolated PGs. However, the activities of HaTreh1 and HaTreh2 triggered by PBAN were offset by H-89 2HCl, the specific inhibitor of protein kinase A (PKA). Furthermore, the H-89 2HCl treatment significantly decreased the phosphorylation level of Trhe2, which was induced by PBAN[3]. The PKA inhibitor H-89 2HCl potently blocked oncosphere larval motility, as well as the motility of other life stages, although other inhibitors of the PKA pathway were not effective[7]. H-89 2HCl (0.2 mg/100g) significantly increases seizure latency and threshold in PTZ-treated animals. H-89 2HCl (0.05, 0.2 mg/100 g) prevents the epileptogenic activity of bucladesine with significant increase of seizure latency and seizure threshold[5]. References: |
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