mouse anti c myc antibody  (Cell Signaling Technology Inc)

Journal: Cell Communication and Signaling : CCS

Article Title: Activation of aryl hydrocarbon receptor alleviates cholestatic liver injury by inhibiting inflammation

doi: 10.1186/s12964-026-02755-w

Figure Lengend Snippet: Proposed working model of AHR signaling in cholestatic liver injury (CLI). Cholestasis is associated with gut microbiota dysbiosis, including a reduced abundance of tryptophan-metabolizing bacteria and an increased abundance of LPS-producing bacteria (e.g., Escherichia-Shigella ). These alterations are accompanied by disrupted tryptophan metabolism and enhanced translocation of microbial products such as LPS to the liver, which are associated with impaired AHR activation and amplified hepatic inflammatory responses, including increased chemokine expression (e.g., CCL2) and recruitment of inflammatory cells. Pharmacological activation of AHR by tryptophan-derived metabolites (such as ITE) or AAV-mediated AHR overexpression attenuates inflammatory responses and liver injury, at least in part through suppression of chemokine expression. Hepatocyte-intrinsic AHR signaling is depicted as one contributing node within a broader multicellular inflammatory network rather than a dominant determinant of disease severity. This schematic represents a proposed working model based on the present findings

Article Snippet: After 12 h of cell starvation, LPS (500 nM, MedChemExpress, Shanghai, China, # HY-D1056) was added, along with ITE (10 nM or 100 nM, MedChemExpress Shanghai, China, # HY-19317), or liposome transfection of AHR overexpression plasmid (1ug/mL, Sino Biological, Beijing, China, # MG50786-CM), and the AHR inhibitor CH223191 (CH) (10 μM, MedChemExpress, Shanghai, China, # HY-12684) was added when necessary.

Techniques: Bacteria, Translocation Assay, Activation Assay, Amplification, Expressing, Derivative Assay, Over Expression