[Ser25] Protein Kinase C (19-31)
(Synonyms: H2N-Arg-Phe-Ala-Arg-Lys-Gly-Ser-Leu-Arg-Gln-Lys-Asn-Val-OH ) 目录号 : GP10017
PKC substrate
![[Ser25] Protein Kinase C (19-31) Chemical Structure](/media/struct/GP1/GP10017.png "[Ser25] Protein Kinase C (19-31) Chemical Structure")
Cas No.:136795-05-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Protein Kinase C (19-31), (C67H118N26O17), a peptide with the sequence H-ARG-PHE-ALA-ARG-LYS-GLY-SER-LEU-ARG-GLN-LYS-ASN-VAL-OH, MW= 1559.82. this peptide derived from the pseudo-substrate regulatory domain of PKCa (residues 19-31) with a serine at position 25 replacing the wild-type alanine, it was used as protein kinase C substrate peptide for testing the protein kinase C activity.
Protein kinase C also known as PKC, is a family of protein kinase enzymes that are involved in controlling the function of other proteins through the phosphorylation of hydroxyl groups of serine and threonine amino acid residues on these proteins. PKCa has been reported to play roles in many different cellular processes, such as cell adhesion, cell transformation, cell cycle checkpoint, and cell volume control. Knockout studies in mice suggest that this kinase may be a fundamental regulator of cardiac contractility and Ca2+ handling in myocytes.
References:
1. Mellor H, Parker PJ (1998). "The extended protein kinase C superfamily". Biochem. J.. 332 ( Pt 2): 281-92
2. Nishizuka Y (1995). "Protein kinase C and lipid signaling for sustained cellular responses" (abstract). FASEB J. 9 (7): 484-96.
3. Vicente Micol. Correlation between Protein Kinase C an Activity and Membrane Phase Behavior. Departamento de Bioqu??mica y Biolog??a Molecular
| Cas No. | 136795-05-6 | SDF | |
| 别名 | H2N-Arg-Phe-Ala-Arg-Lys-Gly-Ser-Leu-Arg-Gln-Lys-Asn-Val-OH | ||
| 化学名 | [Ser25] Protein Kinase C (19-31) | ||
| Canonical SMILES | CC(C)CC(C(=O)NC(CCCN=C(N)N)C(=O)NC(CCC(=O)N)C(=O)NC(CCCCN)C(=O)NC(CC(=O)N)C(=O)NC(C(C)C)C(=O)O)NC(=O)C(CO)NC(=O)CNC(=O)C(CCCCN)NC(=O)C(CCCN=C(N)N)NC(=O)C(C)NC(=O)C(CC1=CC=CC=C1)NC(=O)C(CCCN=C(N)N)N | ||
| 分子式 | C67H118N26O17 | 分子量 | 1559.82 |
| 溶解度 | ≥ 155.9mg/mL in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.6411 mL | 3.2055 mL | 6.411 mL |
| 5 mM | 0.1282 mL | 0.6411 mL | 1.2822 mL |
| 10 mM | 0.0641 mL | 0.3205 mL | 0.6411 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Protein kinase C controls the priming step of regulated exocytosis in adrenal chromaffin cells
1. To investigate the mechanism whereby protein kinase C enhances secretory function in adrenal chromaffin cells, we examined the effects of 12-O-tetradecanoylphorbor-13-acetate (TPA) on Ca(2+)-induced catecholamine release from digitonin-permeabilized cells, resolving the release into a MgATP-dependent priming step and a MgATP-independent Ca(2+)-triggered step. Treatment with TPA selectively potentiated the priming activity of MgATP, with little increase in the MgATP-independent release. The potentiation by TPA of the MgATP-dependent priming was blocked by [Ser25]protein kinase C(19-31), a specific substrate of protein kinase C. G? 6976, an inhibitor selective for protein kinase C alpha and beta isoforms, also blocked the potentiation by TPA. These results suggest that activation of protein kinase C, probably the alpha isoform, potentiates the MgATP-dependent priming step. 2. The antibody raised against GAP-43, a known substrate of protein kinase C, also potentiated the MgATP-dependent priming. The effect of TPA and that of the anti-GAP-43 antibody were not additive. Calmodulin, which binds to GAP-43 and inhibits its phosphorylation by protein kinase C, abolished the effect of TPA. Thus, the present results suggest that protein kinase C potentiates MgATP-dependent priming, at least in part, through phosphorylation of GAP-43.
Alkyllysophospholipid ET-18-OCH3 acts as an activator of protein kinase C in HL-60 cells
HL-60 cells are very sensitive to the cytotoxic action of ether lipids. Several hypotheses have been proposed to explain this cytotoxicity. We investigated the influence of the alkylphospholipid ET-18-OCH3 on the activity of protein kinase C. HL-60 cells were incubated with ET-18-OCH3 at a concentration of 20 micrograms/ml for 4 h. After the incubation the membrane fraction of the HL-60 cells was isolated and the activity of protein kinase C was determined while it was still associated with the membrane, using the synthetic peptide substrate [Ser25]-protein kinase C (19-31) as a protein kinase C specific substrate. The activity of the membrane-bound protein kinase C was increased in HL-60 cells treated with ET-18-OCH3 compared to untreated HL-60 cells. The increase in protein kinase C activity was not a consequence of translocation and appeared to be additive to the effect of the phorbol ester 12-myristate 13-acetate. In contrast, solubilized protein kinase C from HL-60 cells could be inhibited or stimulated in vitro by ET-18-OCH3, dependent on the mode of addition of ET-18-OCH3 and phospholipids.