Ackr3-Venus knock-in mouse lights up brain vasculature.
Ackr3-Venus knock-in mouse lights up brain vasculature.
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DOI:
10.1186/s13041-021-00862-y
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发表时间:
2021-09-28
期刊:
影响因子:
3.6
通讯作者:
Kieffer BL
中科院分区:
文献类型:
--
作者:
Ehrlich AT;Semache M;Couvineau P;Wojcik S;Kobayashi H;Thelen M;Gross F;Hogue M;Le Gouill C;Darcq E;Bouvier M;Kieffer BL
The atypical chemokine receptor 3, ACKR3, is a G protein-coupled receptor, which does not couple to G proteins but recruits βarrestins. At present, ACKR3 is considered a target for cancer and cardiovascular disorders, but less is known about the potential of ACKR3 as a target for brain disease. Further, mouse lines have been created to identify cells expressing the receptor, but there is no tool to visualize and study the receptor itself under physiological conditions. Here, we engineered a knock-in (KI) mouse expressing a functional ACKR3-Venus fusion protein to directly detect the receptor, particularly in the adult brain. In HEK-293 cells, native and fused receptors showed similar membrane expression, ligand induced trafficking and signaling profiles, indicating that the Venus fusion does not alter receptor signaling. We also found that ACKR3-Venus enables direct real-time monitoring of receptor trafficking using resonance energy transfer. In ACKR3-Venus knock-in mice, we found normal ACKR3 mRNA levels in the brain, suggesting intact gene transcription. We fully mapped receptor expression across 14 peripheral organs and 112 brain areas and found that ACKR3 is primarily localized to the vasculature in these tissues. In the periphery, receptor distribution aligns with previous reports. In the brain there is notable ACKR3 expression in endothelial vascular cells, hippocampal GABAergic interneurons and neuroblast neighboring cells. In conclusion, we have generated Ackr3-Venus knock-in mice with a traceable ACKR3 receptor, which will be a useful tool to the research community for interrogations about ACKR3 biology and related diseases. The online version contains supplementary material available at 10.1186/s13041-021-00862-y.
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DOI:
10.1007/s11481-015-9616-y
发表时间:
2016-03
期刊:
Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology
影响因子:
--
作者:
Banisadr G;Podojil JR;Miller SD;Miller RJ
通讯作者:
Miller RJ
DOI:
10.1084/jem.20102010
发表时间:
2011-02-14
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Cruz-Orengo L;Holman DW;Dorsey D;Zhou L;Zhang P;Wright M;McCandless EE;Patel JR;Luker GD;Littman DR;Russell JH;Klein RS
通讯作者:
Klein RS
影响因子:
3.1
作者:
Ehrlich AT;Semache M;Bailly J;Wojcik S;Arefin TM;Colley C;Le Gouill C;Gross F;Lukasheva V;Hogue M;Darcq E;Harsan LA;Bouvier M;Kieffer BL
通讯作者:
Kieffer BL
影响因子:
64.5
作者:
Hauser AS;Chavali S;Masuho I;Jahn LJ;Martemyanov KA;Gloriam DE;Babu MM
通讯作者:
Babu MM
影响因子:
3.1
作者:
EVA, C;SPRENGEL, R
通讯作者:
SPRENGEL, R