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卡弗他丁C

卡弗他丁C用途

钙磷素C是蛋白激酶C的有效和特异性抑制剂。钙磷素C是一种抗肿瘤抗生素。钙磷素C对蛋白激酶C的抑制作用是其他蛋白激酶的1000倍,IC50为0.05μM。钙磷素C在某些肿瘤细胞系中诱导凋亡。钙磷素C具有很强的细胞毒性和抗肿瘤活性[1]。

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卡弗他丁C名称

[ CAS 号 ]:
121263-19-2

[ 中文名 ]:
抑制剂C

[ 英文名 ]:
Calphostin C

[中文别名 ]:

卡弗他丁C

[英文别名 ]:

Calphostin C
MFCD00133155

卡弗他丁C生物活性

[ 描述 ]:

[ 相关类别 ]:

信号通路 >> 表观遗传学 >> PKC

信号通路 >> 细胞凋亡 >> 细胞凋亡

研究领域 >> 癌症

研究领域 >> 感染

信号通路 >> TGF-beta/Smad 信号通路 >> PKC

[ 靶点 ]

protein kinase C[1]

[参考文献]

[1]. Kobayashi E, et al. Calphostin C (UCN-1028C), a novel microbial compound, is a highly potent and specific inhibitor of protein kinase C. Biochem Biophys Res Commun. 1989;159(2):548-553.

[2]. Kobayashi E, et al. Calphostins (UCN-1028), novel and specific inhibitors of protein kinase C. I. Fermentation, isolation, physico-chemical properties and biological activities. J Antibiot (Tokyo). 1989;42(10):1470-1474.

卡弗他丁C物理化学性质

[ 密度 ]:
1.5±0.1 g/cm3

[ 沸点 ]:
1039.8±65.0 °C at 760 mmHg

[ 分子式 ]:
C₄₄H₃₈O₁₄

[ 分子量 ]:
790.764

[ 闪点 ]:
317.0±27.8 °C

[ 精确质量 ]:
790.226135

[ PSA ]:
193.58000

[ LogP ]:
9.15

[ 外观性状 ]:
红色至棕色粉末

[ 蒸汽压 ]:
0.0±0.3 mmHg at 25°C

[ 折射率 ]:
1.705

卡弗他丁CMSDS

详细MSDS(安全技术说明书)

卡弗他丁C安全信息

[ 个人防护装备 ]:
Eyeshields;Gloves;type N95 (US);type P1 (EN143) respirator filter

[ 危害码 (欧洲) ]:
Xn

[ 安全声明 (欧洲) ]:
24/25

[ 危险品运输编码 ]:
NONH for all modes of transport

卡弗他丁C文献

β-Adrenergic receptors activate exchange protein directly activated by cAMP (Epac), translocate Munc13-1, and enhance the Rab3A-RIM1α interaction to potentiate glutamate release at cerebrocortical nerve terminals.

J. Biol. Chem. 288(43) , 31370-85, (2013)

The adenylyl cyclase activator forskolin facilitates synaptic transmission presynaptically via cAMP-dependent protein kinase (PKA). In addition, cAMP also increases glutamate release via PKA-independe...

PPARγ regulates resistance vessel tone through a mechanism involving RGS5-mediated control of protein kinase C and BKCa channel activity.

Circ. Res. 111(11) , 1446-58, (2012)

Activation of peroxisome proliferator-activated receptor-γ (PPARγ) by thiazolidinediones lowers blood pressure, whereas PPARγ mutations cause hypertension. Previous studies suggest these effects may b...

Impairment of neurovascular coupling in type 1 diabetes mellitus in rats is linked to PKC modulation of BK(Ca) and Kir channels.

Am. J. Physiol. Heart Circ. Physiol. 302(6) , H1274-84, (2012)

We hypothesized that chronic hyperglycemia has a detrimental effect on neurovascular coupling in the brain and that this may be linked to protein kinase C (PKC)-mediated phosphorylation. Therefore, in...

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