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CAS No.113276-94-1 5-Isoquinolinesulfonamide,N-[2-(methylamino)ethyl]-, hydrochloride (1:2)

Supplier:Hangzhou Share Chemical Co., Ltd [ China (Mainland)]

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CAS No.113276-94-1 5-Isoquinolinesulfonamide,N-[2-(methylamino)ethyl]-, hydrochloride (1:2)

H-8, Dihydrochloride

Supplier:TRUST&WE CO.,Ltd. [ China (Mainland)]

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CAS No.113276-94-1 5-Isoquinolinesulfonamide,N-[2-(methylamino)ethyl]-, hydrochloride (1:2)

Supplier:HANGZHOU LION BIOTECHNOLOGY CO.,LTD. [ China (Mainland)]

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Address:Zhejiang Province, Hangzhou Economic and Technological Development Zone No. 6, Street 452

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Reference

Protein kinase C activators work in synergy with specific growth factors to initiate tyrosine hydroxylase expression in striatal neurons in culture
Protein kinase C activators work in synergy with specific growth factors to initiate tyrosine hydroxylase expression in striatal neurons in culture. Du, Xinyu; Iacovitti, Lorraine (Department of Neurobiology and Anatomy, Medical College of Pennsylvania and Hahnemann University, Philadelphia, PA, USA). Journal of Neurochemistry, 68(2), 564-569 (English) 1997 Lippincott-Raven. CODEN: JONRA9. ISSN: 0022-3042. DOCUMENT TYPE: Journal CA Section: 13 (Mammalian Biochemistry) The previous studies indicate that, in the noncatecholamine (non-CA) neurons of the striatum, expression of the gene for the CA biosynthetic enzyme tyrosine hydroxylase (TH) can be initiated by the synergistic interaction of acidic fibroblast growth factor (aFGF) and a second partner mol. The aim of this study was to det. whether the activators of protein kinase C (PKC) signaling pathways, either alone or in conjunction with various growth factors, is sufficient to induce TH in striatal neurons. It was found that when the active b form of 4b-12-O-tetradecanoylphorbol 13-acetate (TPA), but not the inactive a analog, was incubated in the presence of aFGF, basic FGF, or brain-derived neurotrophic factor, TH expression was initiated. Activation of the PKC pathways alone (in the absence of growth factors) did not mimic these effects, suggesting that multiple pathway activation is required for novel TH expression. 113276-94-1 and 90365-57-4 are also in the experiment. Although other specific activators of PKC were effective growth factor partners, TPA was the most potent with an ED50 of 0.008 mM. Conversely, inhibitors of protein kinases, such as H7, H8, or H89, prevented the expression of TH by aFGF and TPA. Because pretreatment with protein (cycloheximide) or RNA synthesis (amanitin and actinomycin D) inhibitors eliminated the inductive effect of aFGF and TPA, it is concluded that de novo transcription and translation are necessary for the expression of TH after convergence of both PKC and growth factor pathways. .
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