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Merck
CN

P3115

Sigma-Aldrich

Protein Kinase C Inhibitor, Myristoylated

≥7.5 mg/mL (peptide and counter ion), ≥95% (Minimum peptide content 70%, HPLC), aqueous solution (neutral pH)

Synonym(s):

Myr-Arg-Phe-Ala-Arg-Lys-Gly-Ala-Leu-Arg-Gln-Lys-Asn-Val, Myr-RFARKGALRQKNV

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About This Item

MDL number:
UNSPSC Code:
12352200
NACRES:
NA.77
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biological source

synthetic (organic
organic)

Assay

≥95% (Minimum peptide content 70%, HPLC)

form

aqueous solution (neutral pH)

mol wt

1,754.3 Da (Fast Atomic Bombardment Mass Spectrometry)
1.75 kDa

composition

Peptide content, ≥70%

concentration

≥7.5 mg/mL (peptide and counter ion)

shipped in

dry ice

storage temp.

−20°C

Application

Protein Kinase C (PKC) Inhibitor, Myristoylated is supplied ready for use in kinase reactions. An inhibitor peptide (concentration of 50 to 100 μM) is recommended, depending on the concentration of PKC and the duration of the incubation.

Biochem/physiol Actions

Protein Kinase C Inhibitor, Myristoylated is a cell permeable, specific inhibitor of calcium and phospholipid-dependent Protein Kinase C.

Storage Class Code

10 - Combustible liquids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Regulatory Information

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T Eichholtz et al.
The Journal of biological chemistry, 268(3), 1982-1986 (1993-01-25)
Synthetic peptides corresponding to the pseudosubstrate domains of protein kinase C (PKC) have been used as specific inhibitors of PKC in in vitro assays and permeabilized cell systems. However, their use in vivo was hampered by the impermeability of the
Katarzyna Bialkowska et al.
The Journal of biological chemistry, 290(10), 6226-6242 (2015-01-23)
The contributions of integrins to cellular responses depend upon their activation, which is regulated by binding of proteins to their cytoplasmic tails. Kindlins are integrin cytoplasmic tail binding partners and are essential for optimal integrin activation, and kindlin-3 fulfills this
Hongwei Si et al.
Endocrinology, 153(7), 3190-3198 (2012-06-07)
We previously reported that genistein, a phytoestrogen, up-regulates endothelial nitric oxide synthase (eNOS) and prevents hypertension in rats that are independent of estrogen signaling machinery. However, how genistein regulates eNOS expression is unknown. In the present study, we show that
Samantha L Yuen et al.
American journal of physiology. Heart and circulatory physiology, 297(1), H191-H199 (2009-05-12)
The participation of nonmuscle myosin in force maintenance is controversial. Furthermore, its regulation is difficult to examine in a cellular context, as the light chains of smooth muscle and nonmuscle myosin comigrate under native and denaturing electrophoresis techniques. Therefore, the

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