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由 G 蛋白偶联受体 FPR2 传递的发育和内稳态信号。

Developmental and homeostatic signaling transmitted by the G-protein coupled receptor FPR2.

机构信息

Laboratory of Cancer Innovation, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, USA.

Basic Research Program, Leidos Biomedical Research, Inc., Frederick, MD, USA.

出版信息

Int Immunopharmacol. 2023 May;118:110052. doi: 10.1016/j.intimp.2023.110052. Epub 2023 Mar 30.

DOI:10.1016/j.intimp.2023.110052
PMID:37003185
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10149111/
Abstract

Formyl peptide receptor 2 (FPR2) and its mouse counterpart Fpr2 are the members of the G protein-coupled receptor (GPCR) family. FPR2 is the only member of the FPRs that interacts with ligands from different sources. FPR2 is expressed in myeloid cells as well as epithelial cells, endothelial cells, neurons, and hepatocytes. During the past years, some unusual properties of FPR2 have attracted intense attention because FPR2 appears to possess dual functions by activating or inhibiting intracellular signal pathways based on the nature, concentration of the ligands, and the temporal and spatial settings of the microenvironment in vivo, the cell types it interacts with. Therefore, FPR2 controls an abundant array of developmental and homeostatic signaling cascades, in addition to its "classical" capacity to mediate the migration of hematopoietic and non-hematopoietic cells including malignant cells. In this review, we summarize recent development in FPR2 research, particularly in its role in diseases, therefore helping to establish FPR2 as a potential target for therapeutic intervention.

摘要

形式肽受体 2(FPR2)及其小鼠对应物 Fpr2 是 G 蛋白偶联受体(GPCR)家族的成员。FPR2 是唯一与来自不同来源的配体相互作用的 FPR 成员。FPR2 表达于髓系细胞以及上皮细胞、内皮细胞、神经元和肝细胞。在过去的几年中,FPR2 的一些不寻常特性引起了人们的极大关注,因为 FPR2 似乎具有双重功能,它可以根据配体的性质、浓度以及体内微环境的时空设置,激活或抑制细胞内信号通路,与它相互作用的细胞类型。因此,FPR2 控制着大量的发育和稳态信号级联反应,除了其“经典”能力介导造血和非造血细胞(包括恶性细胞)的迁移。在这篇综述中,我们总结了 FPR2 研究的最新进展,特别是它在疾病中的作用,因此有助于将 FPR2 确立为治疗干预的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ada/10149111/67cfce99a0ce/nihms-1888411-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ada/10149111/0841d9f437b2/nihms-1888411-f0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ada/10149111/cdca2bffddd7/nihms-1888411-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ada/10149111/a0fc2aed2b90/nihms-1888411-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ada/10149111/e9c053826eb9/nihms-1888411-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ada/10149111/67cfce99a0ce/nihms-1888411-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ada/10149111/0841d9f437b2/nihms-1888411-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ada/10149111/1bec0cdd2343/nihms-1888411-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ada/10149111/b0c6a786ae49/nihms-1888411-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ada/10149111/cdca2bffddd7/nihms-1888411-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ada/10149111/a0fc2aed2b90/nihms-1888411-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ada/10149111/e9c053826eb9/nihms-1888411-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ada/10149111/67cfce99a0ce/nihms-1888411-f0007.jpg

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