CCR8 blocking peptide

Name: CCR8 blocking peptide
SKU: CDBP5280
Rating: 5 (1 reviews)

Synthetic CCR8 blocking peptide for IB

COA

SDS

Datasheet

Summary

Nature

Synthetic

Tag/Conjugate

Unconjugated

Format

Liquid

Concentration

200 μg/mL

Preservative

None

Storage

-20°C

Entrez Gene ID

1237

Antigen Description

This gene encodes a member of the beta chemokine receptor family, which is predicted to be a seven transmembrane protein similar to G protein-coupled receptors. Chemokines and their receptors are important for the migration of various cell types into the inflammatory sites. This receptor protein preferentially expresses in the thymus. I-309, thymus activation-regulated cytokine (TARC) and macrophage inflammatory protein-1 beta (MIP-1 beta) have been identified as ligands of this receptor. Studies of this receptor and its ligands suggested its role in regulation of monocyte chemotaxis and thymic cell apoptosis. More specifically, this receptor may contribute to the proper positioning of activated T cells within the antigenic challenge sites and specialized areas of lymphoid tissues. This gene is located at the chemokine receptor gene cluster region. [provided by RefSeq, Jul 2008]

Function

C-C chemokine receptor activity; chemokine receptor activity; coreceptor activity

Synonyms

CCR8; chemokine (C-C motif) receptor 8; CY6; TER1; CCR-8; CKRL1; CDw198; CMKBR8; GPRCY6; CMKBRL2; CC-CKR-8; C-C chemokine receptor type 8; CC chemokine receptor 8; chemokine receptor-like 1; chemokine (C-C) receptor 8; CC chemokine receptor CHEMR1; CC-chemokine receptor chemr1; chemokine (C-C) receptor-like 2

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

A Multistep Continuous-Flow System for Rapid On-Demand Synthesis of Receptor Ligands

ORGANIC LETTERS

Authors: Petersen, Trine P.; Ritzen, Andreas; Ulven, Trond

Abstract

A multistep continuous-flow system for synthesis of receptor ligands by assembly of three variable building blocks in a single unbroken flow is described. The sequence consists of three reactions and two scavenger steps, where a Cbz-protected diamine is reacted with an isocyanate, deprotected, and reacted further with an alkylating agent.

Glycosylated extracellular vesicles released by glioblastoma cells are decorated by CCL18 allowing for cellular uptake via chemokine receptor CCR8

JOURNAL OF EXTRACELLULAR VESICLES

Authors: Berenguer, Jordi; Lagerweij, Tonny; Zhao, Xi Wen; Dusoswa, Sophie; van der Stoop, Petra; Westerman, Bart; de Gooijer, Mark C.; Zoetemelk, Marloes; Zomer, Anoek; Crommentuijn, Matheus H. W.; Wedekind, Laurine E.; Lopez-Lopez, Alan; Giovanazzi, Alberta; Bruch-Oms, Marina; van der Meulen-Muileman, Ida H.; Reijmers, Rogier M.; van Kuppevelt, Toin H.; Garcia-Vallejo, Juan-Jesus; van Kooyk, Yvette; Tannous, Bakhos A.; Wesseling, Pieter; Koppers-Lalic, Danijela; Vandertop, W. Peter; Noske, David P.; van Beusechem, Victor W.; van Rheenen, Jacco; Pegtel, D. Michiel; van Tellingen, Olaf; Wurdinger, Thomas

Abstract

Cancer cells release extracellular vesicles (EVs) that contain functional biomolecules such as RNA and proteins. EVs are transferred to recipient cancer cells and can promote tumour progression and therapy resistance. Through RNAi screening, we identified a novel EV uptake mechanism involving a triple interaction between the chemokine receptor CCR8 on the cells, glycans exposed on EVs and the soluble ligand CCL18. This ligand acts as bridging molecule, connecting EVs to cancer cells. We show that glioblastoma EVs promote cell proliferation and resistance to the alkylating agent temozolomide (TMZ). Using in vitro and in vivo stem-like glioblastoma models, we demonstrate that EV-induced phenotypes are neutralised by a small molecule CCR8 inhibitor, R243. Interference with chemokine receptors may offer therapeutic opportunities against EV-mediated cross-talk in glioblastoma.