Small molecule antagonism of oxysterol-induced Epstein-Barr virus induced gene 2 (EBI2) activation

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Small molecule antagonism of oxysterol-induced Epstein-Barr virus induced gene 2 (EBI2) activation. / Benned-Jensen, Tau; Madsen, Christian M; Arfelt, Kristine N; Smethurts, Christian; Blanchard, Andy; Jepras, Robert; Rosenkilde, Mette M.

In: FEBS Open Bio, Vol. 3, 2013, p. 156-60.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Benned-Jensen, T, Madsen, CM, Arfelt, KN, Smethurts, C, Blanchard, A, Jepras, R & Rosenkilde, MM 2013, 'Small molecule antagonism of oxysterol-induced Epstein-Barr virus induced gene 2 (EBI2) activation', FEBS Open Bio, vol. 3, pp. 156-60. https://doi.org/10.1016/j.fob.2013.02.003

APA

Benned-Jensen, T., Madsen, C. M., Arfelt, K. N., Smethurts, C., Blanchard, A., Jepras, R., & Rosenkilde, M. M. (2013). Small molecule antagonism of oxysterol-induced Epstein-Barr virus induced gene 2 (EBI2) activation. FEBS Open Bio, 3, 156-60. https://doi.org/10.1016/j.fob.2013.02.003

Vancouver

Benned-Jensen T, Madsen CM, Arfelt KN, Smethurts C, Blanchard A, Jepras R et al. Small molecule antagonism of oxysterol-induced Epstein-Barr virus induced gene 2 (EBI2) activation. FEBS Open Bio. 2013;3:156-60. https://doi.org/10.1016/j.fob.2013.02.003

Author

Benned-Jensen, Tau ; Madsen, Christian M ; Arfelt, Kristine N ; Smethurts, Christian ; Blanchard, Andy ; Jepras, Robert ; Rosenkilde, Mette M. / Small molecule antagonism of oxysterol-induced Epstein-Barr virus induced gene 2 (EBI2) activation. In: FEBS Open Bio. 2013 ; Vol. 3. pp. 156-60.

Bibtex

@article{4ca47ed7b6844217aab97b71c589170d,
title = "Small molecule antagonism of oxysterol-induced Epstein-Barr virus induced gene 2 (EBI2) activation",
abstract = "The Epstein-Barr virus induced gene 2 (EBI2) was recently identified as the first oxysterol-activated 7TM receptor. EBI2 is essential for B cell trafficking within lymphoid tissues and thus the humoral immune response in general. Here we characterize the antagonism of the non-peptide molecule GSK682753A, which blocks oxysterol-induced G-protein activation, β-arrestin recruitment and B-cell chemotaxis. We furthermore demonstrate that activation triggers pertussis toxin-sensitive MAP kinase phosphorylation, which is also inhibited by GSK682753A. Thus, EBI2 signalling in B cells mediates key phenotypic functions via signalling pathways amenable to manipulation providing additional therapeutic options for inhibiting EBI2 activity.",
author = "Tau Benned-Jensen and Madsen, {Christian M} and Arfelt, {Kristine N} and Christian Smethurts and Andy Blanchard and Robert Jepras and Rosenkilde, {Mette M}",
year = "2013",
doi = "10.1016/j.fob.2013.02.003",
language = "English",
volume = "3",
pages = "156--60",
journal = "FEBS Open Bio",
issn = "2211-5463",
publisher = "FEBS Press",

}

RIS

TY - JOUR

T1 - Small molecule antagonism of oxysterol-induced Epstein-Barr virus induced gene 2 (EBI2) activation

AU - Benned-Jensen, Tau

AU - Madsen, Christian M

AU - Arfelt, Kristine N

AU - Smethurts, Christian

AU - Blanchard, Andy

AU - Jepras, Robert

AU - Rosenkilde, Mette M

PY - 2013

Y1 - 2013

N2 - The Epstein-Barr virus induced gene 2 (EBI2) was recently identified as the first oxysterol-activated 7TM receptor. EBI2 is essential for B cell trafficking within lymphoid tissues and thus the humoral immune response in general. Here we characterize the antagonism of the non-peptide molecule GSK682753A, which blocks oxysterol-induced G-protein activation, β-arrestin recruitment and B-cell chemotaxis. We furthermore demonstrate that activation triggers pertussis toxin-sensitive MAP kinase phosphorylation, which is also inhibited by GSK682753A. Thus, EBI2 signalling in B cells mediates key phenotypic functions via signalling pathways amenable to manipulation providing additional therapeutic options for inhibiting EBI2 activity.

AB - The Epstein-Barr virus induced gene 2 (EBI2) was recently identified as the first oxysterol-activated 7TM receptor. EBI2 is essential for B cell trafficking within lymphoid tissues and thus the humoral immune response in general. Here we characterize the antagonism of the non-peptide molecule GSK682753A, which blocks oxysterol-induced G-protein activation, β-arrestin recruitment and B-cell chemotaxis. We furthermore demonstrate that activation triggers pertussis toxin-sensitive MAP kinase phosphorylation, which is also inhibited by GSK682753A. Thus, EBI2 signalling in B cells mediates key phenotypic functions via signalling pathways amenable to manipulation providing additional therapeutic options for inhibiting EBI2 activity.

U2 - 10.1016/j.fob.2013.02.003

DO - 10.1016/j.fob.2013.02.003

M3 - Journal article

C2 - 23772388

VL - 3

SP - 156

EP - 160

JO - FEBS Open Bio

JF - FEBS Open Bio

SN - 2211-5463

ER -

ID: 48310696