Difference between revisions of "Part:BBa K3009001"
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− | The human formyl peptide receptor 2 (FPR2) is a G-protein | + | The human formyl peptide receptor 2 (FPR2) is a G-protein coupled receptor which is physiologically expressed on immune cell lineages like neutrophils and T-cells. |
− | + | Among other peptides the FPR2 senses the <i>Staphylococcus aureus</i> toxin PSMα3. It was suggested by Cheung et al 2014 that the binding mechanism relies on the formylated N-terminus of the peptide as well as on the C-terminus. In response to receptor activation FPR2 elicits a signaling cascade depending on calcium ions as second messengers. Ultimately this leads to immune cell activation, secretion of inflammatory cytokines and chemotaxis. All of this is connected with an inflammatory outcome <i>in vivo</i>. The neutrophil activation by FPR2 is therefore an important mechanism of its toxicity because it leads to an aggravation of the inflammation related symptoms in <i>Staphylococcus aureus</i> infection. | |
− | This Biobrick can be used in | + | This Biobrick can be used in signaling studies or the cellular detection of several small formylated amyloidogenic peptides. As a controls two peptides with inhibitory (WRWW4) and activating (WKYMVm) effect on FPR2 are available. |
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<partinfo>BBa_K3009001 parameters</partinfo> | <partinfo>BBa_K3009001 parameters</partinfo> | ||
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+ | ==MIT_MAHE 2020== | ||
+ | '''Summary''' | ||
+ | |||
+ | Formyl peptide receptor (FPR) is a subfamily of G protein-coupled receptors which plays an important role in immunology. Activation of FPRs occurs by binding to specific peptides which triggers activation of FPRs, which leads to signaling events that regulate inflammatory responses. Several studies have shown that binding to FPR2 is a chemotactic signal to attract macrophages and other immune cells to the target site to resolve inflammation. Other studies have shown that the activation of this receptor does not itself cause further production of pro-inflammatory mediators by macrophages. | ||
+ | |||
+ | ==References== | ||
+ | |||
+ | 1. Ong, W. Y., & Chua, J. (2019). Role of formyl peptide receptor 2 (FPR2) in the normal brain and in neurological conditions. Neural regeneration research, 14(12), 2071–2072. https://doi.org/10.4103/1673-5374.262575 |
Latest revision as of 17:59, 23 October 2020
FPR2 receptor
The human formyl peptide receptor 2 (FPR2) is a G-protein coupled receptor which is physiologically expressed on immune cell lineages like neutrophils and T-cells. Among other peptides the FPR2 senses the Staphylococcus aureus toxin PSMα3. It was suggested by Cheung et al 2014 that the binding mechanism relies on the formylated N-terminus of the peptide as well as on the C-terminus. In response to receptor activation FPR2 elicits a signaling cascade depending on calcium ions as second messengers. Ultimately this leads to immune cell activation, secretion of inflammatory cytokines and chemotaxis. All of this is connected with an inflammatory outcome in vivo. The neutrophil activation by FPR2 is therefore an important mechanism of its toxicity because it leads to an aggravation of the inflammation related symptoms in Staphylococcus aureus infection.
This Biobrick can be used in signaling studies or the cellular detection of several small formylated amyloidogenic peptides. As a controls two peptides with inhibitory (WRWW4) and activating (WKYMVm) effect on FPR2 are available.
Sequence and Features
- 10COMPATIBLE WITH RFC[10]
- 12COMPATIBLE WITH RFC[12]
- 21COMPATIBLE WITH RFC[21]
- 23COMPATIBLE WITH RFC[23]
- 25COMPATIBLE WITH RFC[25]
- 1000COMPATIBLE WITH RFC[1000]
MIT_MAHE 2020
Summary
Formyl peptide receptor (FPR) is a subfamily of G protein-coupled receptors which plays an important role in immunology. Activation of FPRs occurs by binding to specific peptides which triggers activation of FPRs, which leads to signaling events that regulate inflammatory responses. Several studies have shown that binding to FPR2 is a chemotactic signal to attract macrophages and other immune cells to the target site to resolve inflammation. Other studies have shown that the activation of this receptor does not itself cause further production of pro-inflammatory mediators by macrophages.
References
1. Ong, W. Y., & Chua, J. (2019). Role of formyl peptide receptor 2 (FPR2) in the normal brain and in neurological conditions. Neural regeneration research, 14(12), 2071–2072. https://doi.org/10.4103/1673-5374.262575