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MIF-2 in distinction to MIF seems to absence the required CXCR-interacting motifs essential for activation, and it can be believed to exert a more selective motion in activating the tissue-protecting CD74 signaling pathway. That said, MIF triggers the CD74/CD44/AMPK receptor signaling pathway, which encourages glucose uptake in cardiomyocytes and shields the heart for the duration of ischemia-reperfusion injury (ninety three, 94). even more research are expected to determine the likely of MIF/MIF-2 as a treatment technique to defend the center from ischemic damage.
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MIF demonstrates chemokine-like perform and was discovered being a ligand of both equally CXCR2 and CXCR4. Binding of MIF to these receptors enhances monocyte recruitment and leukocyte chemotaxis (Figure 1). In human chondrosarcoma cells, this recruitment is mediated by Gαi proteins and PI3K in T mobile adhesion by upregulation in the transcription from the αvβthree integrin via PI3K/AKT/NF-κB signaling in a very CXCR2- and CXCR4-mediated way. nonetheless, molecular mechanisms underlying MIF-mediated receptor signaling even now must be delineated [8]. In another review, it had been claimed that MIF specifically interacts with CXCR2 and CXCR4 to promote the recruitment of inflammatory cells [nine].
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