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Fig. 2 | Journal of Inflammation

Fig. 2

From: The immunological function of CXCR2 in the liver during sepsis

Fig. 2

CXCLs-CXCR1/2 signaling cascades for humans and mice. Macrophages, monocytes, and endothelial cells release inflammatory chemokines. In humans, CXCL1-3, 5–8, and in mice, Cxcl-3, 5, 7, are released that bind to human CXCR1 and 2 or murine Cxcr2 in responsive cells (e.g., neutrophils, hepatocytes, and stellate cells). Once activated by CXCLs, the receptor dissociates with the G-protein with the release of the Gβγ subunits from the Gα subunit, which causes activation of phospholipase C (PLC, β-2 isoform) and subsequent calcium mobilization from the endoplasmic reticulum to cytosol and activation of protein kinase C, which lead to increased protein phosphorylation and calcium-binding. While for the Gβγ subunits, adenylate cyclase is inhibited, resulting in decreased cyclic AMP production and subsequent protein kinase A, with increased protein phosphorylation as well. In addition, β-arrestin1/2 regulates receptor internalization with MAP kinase and subsequently drives cell degranulation and receptor internalization for further degradation or recycling

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