Fas C- Terminal Tripeptide
(Synonyms: Ac-Ser-Leu-Val-OH ) 目录号 : GP10123
AC-SER-LEU-VAL-OH
Cas No.:189109-90-8
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
Fas C- Terminal Tripeptide,(C16H29N3O6), a tri-peptide with the sequence AC-SER-LEU-VAL-OH, it’s the C-terminal tripeptide of Fas, MW= 359.4. Fas (APO-1/CD95) is a cell surface receptor, which is a member of the tumor necrosis factor receptor (TNFR) superfamily, The Fas receptor is a death receptor on the surface of cells that leads to programmed cell death (apoptosis). It is one of two apoptosis pathways. Fas forms the death-inducing signaling complex (DISC) upon ligand binding. Upon ensuing death domain (DD) aggregation, the receptor complex is internalized via the cellular endosomal machinery. This allows the adaptor molecule FADD to bind the death domain of Fas through its own death domain. FADD also contains a death effector domain (DED) near its amino terminus,which facilitates binding to the DED of FADD-like interleukin-1 beta-converting enzyme (FLICE), more commonly referred to as caspase-8. FLICE can then self-activate through proteolytic cleavage into p10 and p18 subunits, two each of which form the active heterotetramer enzyme. Active caspase-8 is then released from the DISC into the cytosol, where it cleaves other effector caspases, eventually leading to DNA degradation, membrane blebbing, and other hallmarks of apoptosis.
The C-terminal tripeptide (AC-SER-LEU-VAL-OH) of Fas was necessary and sufficient both for binding to the third PDZ domain of FAP-1 and for inhibiting Fas/FAP-1 binding.
References:
1. Lichter P, Walczak H, Weitz S, Behrmann I, Krammer PH (September 1992). "The human APO-1 (APT) antigen maps to 10q23, a region that is syntenic with mouse chromosome 19". Genomics 14 (1): 179–80.
2. Inazawa J, Itoh N, Abe T, Nagata S (November 1992). "Assignment of the human Fas antigen gene (Fas) to 10q24.1". Genomics 14 (3): 821–2.
3. Huang B, et al. (1996). "NMR structure and mutagenesis of the Fas (APO-1/CD95) death domain". Nature 384 (6610): 638–41.
4. Eberstadt M, et al. (1998). "NMR structure and mutagenesis of the FADD (Mort1) death-effector domain". Nature 392 (6679): 941–5.
| Cas No. | 189109-90-8 | SDF | |
| 别名 | Ac-Ser-Leu-Val-OH | ||
| Canonical SMILES | CC(N[C@@H](CO)C(N[C@@H](CC(C)C)C(N[C@@H](C(C)C)C(O)=O)=O)=O)=O | ||
| 分子式 | C16H29N3O6 | 分子量 | 359.42 |
| 溶解度 | ≥ 35.9mg/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 | 2.7823 mL | 13.9113 mL | 27.8226 mL |
| 5 mM | 0.5565 mL | 2.7823 mL | 5.5645 mL |
| 10 mM | 0.2782 mL | 1.3911 mL | 2.7823 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。
Structural modification of Fas C-terminal tripeptide and its effects on the inhibitory activity of Fas/FAP-1 binding
We report the structural requirements of the C-terminal tripeptide derivative of Fas (Ac-Ser-Leu-Val-OH, 1) for the inhibitory activity of Fas/FAP-1 binding. The presence of a carboxyl group and a L-Val residue at the C-terminus is essential for the inhibitory activity, and the hydroxyl group of Ser plays an important role as the donor of a hydrogen bond. The introduction of hydrophobic groups to the N-terminal region of 1, especially the phenylaminocarbonyl group (41), showed a remarkable increase in potency. Further improvement was observed by the attachment of the Glu residue to the meta-position of the phenyl ring of 41 (51). The ester derivative of 41 (56) had the ability to induce apoptosis which was dependent on the concentration of anti-Fas antibody in the colon cancer cell line, DLD-1, which expresses both Fas and FAP-1 and is resistant to Fas-induced apoptosis. We are now investigating whether FAP-1 is a main target of 56 and whether the inhibition of Fas/FAP-1 binding by 56 retrieves the apoptotic signal.
The molecular interaction of Fas and FAP-1. A tripeptide blocker of human Fas interaction with FAP-1 promotes Fas-induced apoptosis
Fas (APO-1/CD95), which is a member of the tumor necrosis factor receptor superfamily, is a cell surface receptor that induces apoptosis. A protein tyrosine phosphatase, Fas-associated phosphatase-1 (FAP-1), that was previously identified as a Fas binding protein interacts with the C-terminal 15 amino acids of the regulatory domain of the Fas receptor. To identify the minimal region of the Fas C-terminal necessary for binding to FAP-1, we employed an in vitro inhibition assay of Fas/FAP-1 binding using a series of synthetic peptides as well as a screen of random peptide libraries by the yeast two-hybrid system. The results showed that the C-terminal three amino acids (SLV) of human Fas were necessary and sufficient for its interaction with the third PDZ (GLGF) domain of FAP-1. Furthermore, the direct cytoplasmic microinjection of this tripeptide (Ac-SLV) resulted in the induction of Fas-mediated apoptosis in a colon cancer cell line that expresses both Fas and FAP-1. Since t(S/T)X(V/L/I) motifs in the C termini of several other receptors have been shown to interact with PDZ domain in signal transducing molecules, this may represent a general motif for protein-protein interactions with important biological functions.