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. 2021 Nov 15;22(22):12326. doi: 10.3390/ijms222212326

Figure 3.

Figure 3

Schematic model representing the cellular localization, the molecular mechanisms and the effects of AhR activation after cerebral and cardiac ischemia. Under unbounded state, AhR is retained in the cytoplasm in an inactive complex. After ligand binding, AIP is released from the complex and the ligand-AhR-HSP90-p23-Scr structure translocates into the nucleus. Inside the nucleus, the ligand-AhR structure is released from the complex and heterodimerizes with the aryl hydrocarbon receptor nuclear translocator (ARNT) and interacts with the xenobiotics response element (XRE) (1), regulating the expression of several phase I and phase II metabolizing enzymes. The ligand-AhR-ARNT (2) and ligand-AhR (3) can interact with other transcription factors (e.g., NF-kB and the estrogen receptor ER), binding to their response elements (RE) and modulating the expression of their target genes. AhR signaling also includes non-genomic pathways: AhR can function as an E3 ubiquitin ligase (4), while the release of the c-Src kinase (5) results in the phosphorylation of multiple targets.