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Merck
CN
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主要文件

539522

Sigma-Aldrich

PKCε Translocation Inhibitor Peptide

The PKCε Translocation Inhibitor Peptide, Negative Control controls the biological activity of PKCε. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.

别名:

PKCε Translocation Inhibitor Peptide, Protein Kinase Cε Translocation Inhibitor I, EAVSLKPT, PKCε Translocation Inhibitor I, PKCε-RACK2 Interaction Inhibitor I

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About This Item

经验公式（希尔记法）:
C37H65N9O13
分子量:
843.96
UNSPSC代码:
12352202
NACRES:
NA.77

质量水平

100

方案

≥97% (HPLC)

表单

lyophilized solid

制造商/商品名称

Calbiochem®

储存条件

OK to freeze
desiccated (hygroscopic)

颜色

white

溶解性

water: 3 mg/mL

运输

ambient

储存温度

2-8°C

一般描述

An octapeptide that selectively inhibits the translocation of PKCε to subcellular sites. Inhibition of PKCε translocation is known to specifically block phorbol ester or norepinephrine-mediated regulation of contraction in cardiomyocytes.
An octapeptide that selectively inhibits the translocation of protein kinase Cε to subcellular sites in a reversible manner. Inhibition of PKCε translocation is known to specifically block phorbol ester- or norepinephrine-mediated regulation of contraction in cardiomyocytes.

生化/生理作用

Cell permeable: no
Primary Target
PKCε Translocation
Product does not compete with ATP.
Reversible: yes

警告

Toxicity: Standard Handling (A)

序列

H-Glu-Ala-Val-Ser-Leu-Lys-Pro-Thr-OH

外形

Supplied as a trifluoroacetate salt.

重悬

Following reconstitution, aliquot and freeze (-20°C) for long-term storage. Stock solutions are stable for up to 6 months at -20°C.

其他说明

Yedovitzky, M., et al. 1997. J. Biol. Chem. 272, 1417.
Johnson, J.A., et al. 1996. J. Biol. Chem.271, 24962.

法律信息

Sold under license of U.S. Patent 5,783,405.
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

储存分类代码

11 - Combustible Solids

WGK

WGK 1

闪点(°F)

Not applicable

闪点(°C)

Not applicable

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Wattamon Srisakuldee et al.
Cells, 10(10) (2021-10-24)
Mitochondria, abundant organelles in high energy demand cells such as cardiomyocytes, can determine cell death or survival by regulating the opening of mitochondrial permeability transition pore, mPTP. We addressed the hypothesis that the growth factor FGF2, known to reside in
Neus Garcia et al.
Molecular neurobiology, 59(7), 4044-4064 (2022-04-28)
During the nervous system development, synapses are initially overproduced. In the neuromuscular junction (NMJ) however, competition between several motor nerve terminals and the synapses they made ends with the maturation of only one axon. The competitive signaling between axons is

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