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Merck
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主要文件

100065

Sigma-Aldrich

二苯基硼酸-2-氨基乙酯

≥97% (titration), crystalline solid, Ins(1,4,5)P3-induced Ca2+ release inhibitor, Calbiochem®

别名:

二苯基硼酸-2-氨基乙酯, 2-氨基乙氧基二苯基硼酸酯,(2-氨基乙氧基)二苯基硼烷

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About This Item

经验公式(希尔记法):
C14H16BNO
CAS号:
分子量:
225.09
MDL编号:
UNSPSC代码:
12352200
NACRES:
NA.77

产品名称

二苯基硼酸-2-氨基乙酯, A cell-permeable modulator of Ins(1,4,5)P3-induced Ca2+ release.

质量水平

方案

≥97% (titration)

表单

crystalline solid

制造商/商品名称

Calbiochem®

储存条件

OK to freeze
desiccated (hygroscopic)

颜色

white

溶解性

DMSO: 20 mg/mL
95% ethanol: 25 mg/mL

运输

ambient

储存温度

2-8°C

SMILES字符串

B(OCCN)(c2ccccc2)c1ccccc1

InChI

1S/C14H16BNO/c16-11-12-17-15(13-7-3-1-4-8-13)14-9-5-2-6-10-14/h1-10H,11-12,16H2

InChI key

BLZVCIGGICSWIG-UHFFFAOYSA-N

一般描述

Ins(1,4,5)P3诱导Ca2+释放的细胞渗透性调节剂。可抑制大鼠小脑微粒体中Ins(1,4,5)P3诱导的Ca2+释放(IC50 = 42 µM),且不会影响[3H]-Ins(1,4,5)P3 与其受体的结合。其对Ca2+从对精氨酸敏感的Ca2+库(由大鼠腿部骨骼肌和心脏中制备得到)中释放没有影响。可抑制子宫收缩剂诱导的自发性收缩和相位收缩。也有报道其可抑制血管紧张素Ⅱ诱导的主动脉收缩。
Ins(1,4,5)P3诱导Ca2+释放的细胞渗透性调节剂。可抑制大鼠小脑微粒体中Ins(1,4,5)P3诱导的Ca2+释放(IC50 = 42 µM),且不会影响[3H]-Ins(1,4,5)P3 与其受体的结合。在肝细胞中,2-APB可通过一种可能涉及其与通道蛋白或相关调节蛋白结合的机制,来抑制Ca2+库通道。其对Ca2+从对精氨酸敏感的Ca2+库(由大鼠腿部骨骼肌和心脏中制备得到)中释放没有影响。

生化/生理作用

主要靶标
Ins(1,4,5)P3诱导的Ca2+释放
产物不与ATP竞争。
可逆:否
细胞可渗透性:具有
靶标IC50:42 µM,抑制Ins(1,4,5)P3诱导的大鼠小脑微粒体制剂中Ca2+的释放

包装

用惰性气体包装

警告

毒性:标准处理(A)

重悬

溶解后,等分并冷冻保存(-20°C)。储备溶液在-20°C下可稳定保存2个月。

其他说明

Brooke, R. T., et al. 2004.Lab. Invest.84, 29.
Gregory, R.B., et al. 2001.Biochem.J.354, 285.
Ma, H.T., et al. 2001.J. Biol. Chem.276, 18888.
Ascher-Landsberg, S., et al. 1999.Biochem.Biophys.Res. Commun.264, 979.
Maruyama, T., et al. 1997.J. Biochem.122, 498.

法律信息

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

象形图

Exclamation mark

警示用语:

Warning

危险声明

危险分类

Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3

靶器官

Respiratory system

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable


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Journal of Alzheimer's disease : JAD, 75(1), 119-138 (2020-04-07)
Cerebrovascular pathology is pervasive in Alzheimer's disease (AD), yet it is unknown whether cerebrovascular dysfunction contributes to the progression or etiology of AD. In human subjects and in animal models of AD, cerebral hypoperfusion and hypometabolism are reported to manifest
Kazuhiro Takano et al.
Development, growth & differentiation, 53(1), 37-47 (2011-01-26)
This study investigated the development of Ca²(+) signaling mechanisms and their role in initiating morphogenetic cell movement in the presumptive ectoderm of Japanese newt (Cynops pyrrhogaster) during gastrulation. Histochemical staining using fluorescently labeled ryanodine and dihydropyridine probes revealed that dihydropyridine
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Ca2+ influx into the trans-Golgi Network (TGN) promotes secretory cargo sorting by the Ca2+-ATPase SPCA1 and the luminal Ca2+ binding protein Cab45. Cab45 oligomerizes upon local Ca2+ influx, and Cab45 oligomers sequester and separate soluble secretory cargo from the bulk
Mavis A A Tenkorang et al.
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Oxidative stress (OS) is a common characteristic of several neurodegenerative disorders, including Parkinson disease (PD). PD is more prevalent in men than in women, indicating the possible involvement of androgens. Androgens can have either neuroprotective or neurodamaging effects, depending on
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The ubiquitous Ca2+ release-activated Ca2+ (CRAC) channel is crucial to many physiological functions. Both gain and loss of CRAC function is linked to disease. While ORAI1 is a crucial subunit of CRAC channels, recent evidence suggests that ORAI2 and ORAI3

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