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It was shown that aged or/and damaged RBCs are sequestrated in the hepatic sinusoid in a PS-dependent way, and the human sinonasal epithelial cells (HSECs) mediate the recognition and the binding of damaged RBCs in a PS-dependent manner via stabilin-1 and stabilin-2 (pro-phagocytic signals and ligandligand interactions) [275,276,277]

In the presence of bound Wnt ligands, degradation is prevented and -catenin is free to translocate to the nucleus and combine with transcription factors TCF/LEF to initiate the transcription of Wnt target genes (Logan and Nusse, 2004)

The available evidence suggests that AFs could non-covalently bind to HSA binding cavities (185)

Protein tyrosine phosphatase 1B (PTP1B) forms an essential component of these pathways in which it acts as a negative regulator of both leptin and insulin signaling