Rac1 Inhibitor F56, control peptideControl peptide version of Rac1 Inhibitor W56 CAS# 1315378-77-8 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 1315378-77-8 | SDF | Download SDF |
| PubChem ID | 90488751 | Appearance | Powder |
| Formula | C72H116N18O23S | M.Wt | 1633.9 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | Soluble to 1 mg/ml in water | ||
| Sequence | MVDGKPVNLGLFDTAG | ||
| Chemical Name | (3S)-3-[[(2S)-2-[[(2S)-2-[[2-[[(2S)-2-[[(2S)-4-amino-2-[[(2S)-2-[[(2S)-1-[(2S)-6-amino-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-amino-4-methylsulfanylbutanoyl]amino]-3-methylbutanoyl]amino]-3-carboxypropanoyl]amino]acetyl]amino]hexanoyl]pyrrolidine-2-carbonyl]amino]-3-methylbutanoyl]amino]-4-oxobutanoyl]amino]-4-methylpentanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]-3-phenylpropanoyl]amino]-4-[[(2S,3R)-1-[[(2S)-1-(carboxymethylamino)-1-oxopropan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-4-oxobutanoic acid | ||
| SMILES | CC(C)CC(C(=O)NC(CC1=CC=CC=C1)C(=O)NC(CC(=O)O)C(=O)NC(C(C)O)C(=O)NC(C)C(=O)NCC(=O)O)NC(=O)CNC(=O)C(CC(C)C)NC(=O)C(CC(=O)N)NC(=O)C(C(C)C)NC(=O)C2CCCN2C(=O)C(CCCCN)NC(=O)CNC(=O)C(CC(=O)O)NC(=O)C(C(C)C)NC(=O)C(CCSC)N | ||
| Standard InChIKey | DYGBZJOTQUWNJM-BHRKYZIESA-N | ||
| Standard InChI | InChI=1S/C72H116N18O23S/c1-35(2)26-44(62(103)76-33-53(94)81-45(27-36(3)4)64(105)83-46(28-41-18-13-12-14-19-41)65(106)84-49(31-55(97)98)67(108)89-59(40(10)91)71(112)79-39(9)60(101)78-34-56(99)100)82-66(107)47(29-51(75)92)85-70(111)58(38(7)8)88-68(109)50-21-17-24-90(50)72(113)43(20-15-16-23-73)80-52(93)32-77-63(104)48(30-54(95)96)86-69(110)57(37(5)6)87-61(102)42(74)22-25-114-11/h12-14,18-19,35-40,42-50,57-59,91H,15-17,20-34,73-74H2,1-11H3,(H2,75,92)(H,76,103)(H,77,104)(H,78,101)(H,79,112)(H,80,93)(H,81,94)(H,82,107)(H,83,105)(H,84,106)(H,85,111)(H,86,110)(H,87,102)(H,88,109)(H,89,108)(H,95,96)(H,97,98)(H,99,100)/t39-,40+,42-,43-,44-,45-,46-,47-,48-,49-,50-,57-,58-,59-/m0/s1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Control peptide version of Rac1 Inhibitor W56; comprises residues 45-60 of Rac1 with Trp56 replaced by Phe. Does not affect GEF-Rac1 interaction. |
Rac1 Inhibitor F56, control peptide Dilution Calculator
Rac1 Inhibitor F56, control peptide Molarity Calculator
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Trp(56) of rac1 specifies interaction with a subset of guanine nucleotide exchange factors.[Pubmed:11595749]
J Biol Chem. 2001 Dec 14;276(50):47530-41.
Signaling specificity of Rho GTPase pathways is achieved in part by selective interaction between members of the Dbl family guanine nucleotide exchange factors (GEFs) and their Rho GTPase substrates. For example, Trio, GEF-H1, and Tiam1 are a subset of GEFs that specifically activate Rac1 but not the closely related Cdc42. The Rac1 specificity of these GEFs appears to be governed by Rac1-GEF binding interaction. To understand the detailed mechanism underlying the GEF specificity issue, we have analyzed a panel of chimeras made between Rac1 and Cdc42 and examined a series of point mutants of Rac1 made at the switch I, switch II, and beta(2)/beta(3) regions for their ability to interact with and to be activated by the GEFs. The results reveal that Rac1 residues of both the switch I and switch II regions are involved in GEF docking and GEF-mediated nucleotide disruption, because mutation of Asp(38), Asn(39), Gln(61), Tyr(64), or Arg(66)/Leu(67) into Ala results in the loss of GEF binding, whereas mutation at Tyr(32), Asp(65), or Leu(70)/Ser(71) leads to the loss of GEF catalysis while retaining the binding capability. The region between amino acids 53-72 of Rac1 is required for specific recognition and activation by the GEFs, and Trp(56) in beta(3) appears to be the critical determinant. Introduction of Trp(56) to Cdc42 renders it fully responsive to the Rac-specific GEF in vitro and in cells. Further, a polypeptide derived from the beta(3) region of Rac1 including the Trp(56) residue serves as a specific inhibitor for Rac1 interaction with the GEFs. Taken together, these results indicate that Trp(56) is the necessary and sufficient determinant of Rac1 for discrimination by the subset of Rac1-specific GEFs and suggest that a compound mimicking Trp(56) action could be explored as an interfering reagent specifically targeting Rac1 activation.
