T-cadherin, a major adiponectin binding partner, suppresses ERK signaling in metabolic tissues - PubMed
4 days ago
- #ERK signaling
- #adiponectin
- #T-cadherin
- T-cadherin is a major adiponectin binding partner with organ-protective effects.
- T-cadherin suppresses ERK signaling in cultured cells and murine tissues.
- Knockdown of T-cadherin increases ERK phosphorylation in C2C12 myocytes and F2 endothelial cells, while overexpression suppresses it.
- Proteomic analysis shows T-cadherin knockdown upregulates ERK signaling downstream proteins in myocytes.
- T-cadherin knockout affects membrane proteins like IGF1R and EGFR, altering signal transduction.
- T-cadherin ablation in mice increases ERK signaling, leading to cardiac hypertrophy and impaired muscle atrophy during starvation.
- T-cadherin, maintained by adiponectin, regulates intracellular signaling, muscle homeostasis, and exosome production.