Pub. Date : 2021 Aug
PMID : 33864571
5 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Upregulated SOCC and IP3R calcium channels and subsequent elevated cytoplasmic calcium signaling promote nonalcoholic fatty liver disease by inhibiting autophagy. | Calcium | inositol 1,4,5-trisphosphate receptor type 3 | Homo sapiens |
| 2 | Nonalcoholic fatty liver disease (NAFLD) is related to elevated cytoplasmic calcium signaling in hepatocytes, which may be mediated by store-operated calcium channel (SOCC) and inositol triphosphate receptor (IP3R). | Calcium | inositol 1,4,5-trisphosphate receptor type 3 | Homo sapiens |
| 3 | In the OOA model, upregulated extracellular regulated protein kinases 1/2 (ERK1/2), which can be regulated by SOCC and IP3R proteins transient receptor potential canonical 1 (TRPC1)/IP3R with elevated cytoplasmic calcium signaling, over-inhibited forkhead/winged helix O (FOXO) signaling and over-activated mammalian target of rapamycin complex 1 (mTORC1) signaling. | Calcium | inositol 1,4,5-trisphosphate receptor type 3 | Homo sapiens |
| 4 | In the OOA model, upregulated extracellular regulated protein kinases 1/2 (ERK1/2), which can be regulated by SOCC and IP3R proteins transient receptor potential canonical 1 (TRPC1)/IP3R with elevated cytoplasmic calcium signaling, over-inhibited forkhead/winged helix O (FOXO) signaling and over-activated mammalian target of rapamycin complex 1 (mTORC1) signaling. | Calcium | inositol 1,4,5-trisphosphate receptor type 3 | Homo sapiens |
| 5 | Our findings indicate that upregulated SOCC and IP3R channels and subsequent elevated cytoplasmic calcium signaling in hepatocyte fatty lesions inhibits hepatocyte autophagy through (TRPC1/IP3R)/ERK/(FOXO/mTORC1) signaling pathways, causes lipid accumulation and degeneration in hepatocytes, and promotes NAFLD occurrence and development. | Calcium | inositol 1,4,5-trisphosphate receptor type 3 | Homo sapiens |