Fmoc-L-Lys(Heptanoyl)-OH
Need Assistance?
  • US & Canada:
    +
  • UK: +

Fmoc-L-Lys(Heptanoyl)-OH

* Please kindly note that our products are not to be used for therapeutic purposes and cannot be sold to patients.

Category
Fmoc-Amino Acids
Catalog number
BAT-001096
CAS number
1528622-16-3
Molecular Formula
C28H36N2O5
Molecular Weight
480.59
IUPAC Name
(2S)-2-(9H-fluoren-9-ylmethoxycarbonylamino)-6-(heptanoylamino)hexanoic acid
Synonyms
N-alpha-(9-Fluorenylmethyloxycarbonyl)-N-epsilon-heptanoyl-L-lysine; Fmoc-Lys(Heptanoyl); Fmoc-L-Lys(Heptanoyl); Fmoc-HepoK; (2S)-2-({[(9H-fluoren-9-yl)methoxy]carbonyl}amino)-6-heptanamidohexanoic acid
Storage
Store at 2-8 °C
InChI
InChI=1S/C28H36N2O5/c1-2-3-4-5-17-26(31)29-18-11-10-16-25(27(32)33)30-28(34)35-19-24-22-14-8-6-12-20(22)21-13-7-9-15-23(21)24/h6-9,12-15,24-25H,2-5,10-11,16-19H2,1H3,(H,29,31)(H,30,34)(H,32,33)/t25-/m0/s1
InChI Key
PIQLQGXMHXKYPS-VWLOTQADSA-N
Canonical SMILES
CCCCCCC(=O)NCCCCC(C(=O)O)NC(=O)OCC1C2=CC=CC=C2C3=CC=CC=C13
1. [Influences of abaR gene on biofilm formation of Acinetobacter baumannii]
H N Guo, J Xiang Zhonghua Shao Shang Za Zhi. 2017 Apr 20;33(4):200-205. doi: 10.3760/cma.j.issn.1009-2587.2017.04.003.
Objective: To detect drug-resistant phenotype and abaR gene of Acinetobacter baumannii (AB) and investigate influences of abaR gene on biofilm formation of AB. Methods: From February to July 2014, 159 strains AB were collected from Department of Clinical Microbiology of Ruijin Hospital of School of Medicine of Shanghai JiaoTong University and numbered starting from 1 according time when they were collected.
2. Human TRPV1 and TRPA1 are receptors for bacterial quorum sensing molecules
Naoya Tobita, Kana Tsuneto, Shigeaki Ito, Takeshi Yamamoto J Biochem. 2022 Jan 7;170(6):775-785. doi: 10.1093/jb/mvab099.
In this study, we investigated the activation of TRPV1 and TRPA1 by N-acyl homoserine lactones, quorum sensing molecules produced by Gram-negative bacteria, and the inhibitory effect of TRPV1 and TRPA1 by autoinducing peptides (AIPs), quorum sensing molecules produced by Gram-positive bacteria, using human embryonic kidney 293T cell lines stably expressing human TRPV1 and TRPA1, respectively. As a result, we found that some N-acyl homoserine lactones, such as N-octanoyl-L-homoserine lactone (C8-HSL), N-nonanoyl-L-homoserine lactone (C9-HSL) and N-decanoyl-L-homoserine lactone (C10-HSL), activated both TRPV1 and TRPA1. In addition, we clarified that some N-acyl homoserine lactones, such as N-3-oxo-dodecanoyl-L-homoserine lactone (3-oxo-C12-HSL), only activated TRPV1 and N-acyl homoserine lactones having saturated short acyl chain, such as N-acetyl-L-homoserine lactone (C2-HSL) and N-butyryl-L-homoserine lactone (C4-HSL), only activated TRPA1. Furthermore, we found that an AIP, simple linear peptide CHWPR, inhibited both TRPV1 and TRPA1 and peptide having thiolactone ring DICNAYF, the thiolactone ring were formed between C3 to F7, strongly inhibited only the TRPV1. Although the specificity of TRPV1 and TRPA1 for quorum sensing molecules was different, these data suggest that both TRPV1 and TRPA1 would function as receptors for quorum sensing molecule produced by bacteria. Graphical Abstract.
3. Lipid metabolism is differentially modulated by salicylic acid and heptanoyl salicylic acid during the induction of resistance in wheat against powdery mildew
Christine Tayeh, Béatrice Randoux, Natacha Bourdon, Philippe Reignault J Plant Physiol. 2013 Dec 15;170(18):1620-9. doi: 10.1016/j.jplph.2013.06.015. Epub 2013 Jul 20.
Heptanoyl salicylic acid (HSA) is a salicylic acid (SA) derivative obtained by esterification of 2-OH benzoic acid with heptanoic acid. In wheat, the protection levels obtained against Blumeria graminis f. sp. tritici (Bgt) increased from 50% with SA to 95% with HSA. Using molecular, biochemical and cytological approaches, we investigated here how wheat lipid metabolism is differentially activated by SA and HSA in both infectious and non-infectious conditions, and how Bgt infectious process is altered by both inducers. First, in the absence of Bgt, continuous lipoxygenase (LOX)-encoding gene expression and corresponding activity were specifically induced by HSA. Moreover, compared to SA, HSA treatment resulted in earlier up-regulations of the phospholipase C2-encoding gene expression and it specifically affected the expression of a lipid transfer protein-encoding gene. In infectious context, both HSA and SA sprayings impaired penetration events and therefore haustorium formation, leading to less frequent fungal colonies. While this alteration only slowed down the evolution of Bgt infectious process in SA-sprayed leaves, it completely impaired the establishment of successful infectious events in HSA-sprayed leaves. In addition, HSA induced continuous increases of a LOX-encoding gene expression and of the corresponding LOX activity when compared to SA-sprayed leaves. Lipid metabolism is therefore overall highly responsive to HSA spraying and could represent effective defence mechanism triggered during the induction of resistance in wheat toward Bgt. The concepts of priming and energy costs of the defences induced by SA and HSA are also discussed.
Online Inquiry
Verification code
Inquiry Basket