CXCR2

CXCR2

A gene on chromosome 2q35 that encodes a seven-transmembrane G protein-coupled receptor belonging to the CXC chemokine receptor family, which selectively binds IL8, as well as CXCL1, CXCL3, GRO/MGSA and NAP-2. CXCR2 is a potent neutrophil chemotactic factor and mediates neutrophil migration to sites of inflammation; it mediates IL8’s angiogenic effects on intestinal microvascular endothelial cells.
References in periodicals archive ?
28) Thus, although neutrophils are prevented from entering lymph nodes via HEVs under physiological conditions, they can migrate into lymph nodes abundantly when HEVs undergo an inflammation-induced molecular switch, which initiates the neutrophils' CXCR2 engagement by CXCL2 displayed on ECs.
Moreover, these effects of IL-33 involve induction of IL-6, CXCR2 utilizing chemokines, such as CXCL1 and CXCL2, and secretion of type 2 cytokines (Barlow et al.
2014) reported similar results for Murrah buffalo after sequencing and phylogenetic analysis of CXCR2 gene controlling genetic resistance against mastitis.
Autocrine regulation of re-epithelialization after wounding by chemokine receptors CCR1, CCR10, CXCR1, CXCR2, and CXCR3.
A protein called CXCR2 helps pancreatic cancer spread around the body.
Entre ellos se encuentran farmacos tales como el antagonista selectivo del receptor CXCR2, el salicilato de sodio via intraperitoneal, la betanina y la ulinastatina (16-20).
In previous studies, chemokine receptors, such as CXCR2 and CCR4, were genetically modified to be expressed on T cells to enhance their homing and antitumor activity [54, 55].
Hegde, "Treatment with antileukinate, a CXCR2 chemokine receptor antagonist, protects mice against acute pancreatitis and associated lung injury," Regulatory Peptides, vol.
Other GPCRs that stimulate invasion with extracellular signal-regulated kinase (ERK) and matrix metalloproteinase 9 (MMP-9) activation include chemokine (C-X-C motif) receptors CXCR1 and CXCR2 (56,57) and CXCR4.
Arrestin regulates MAPK activation and prevents NADPH oxidase-dependent death ofcells expressing CXCR2.
The researchers found that LukED latches onto surface receptors called CXCR1 and CXCR2, creating the same deadly pores that it does when it latches onto CCR5 receptors.