Title : Integrin alpha5-induced EGFR activation by prothrombin triggers hepatocyte apoptosis via the JNK signaling pathway.

Pub. Date : 2008 Aug

PMID : 18330891






5 Functional Relationships(s)
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1 We found that prothrombin treatment of rat hepatocytes without addition of any growth factor induced tyrosine phosphorylation of integrin alpha5 and interaction of integrin alpha5 with epidermal growth factor receptor (EGFR), leading to EGFR tyrosine phosphorylation at tyrosine residues Tyr-845 and Tyr-1173. Tyrosine epidermal growth factor receptor Rattus norvegicus
2 We found that prothrombin treatment of rat hepatocytes without addition of any growth factor induced tyrosine phosphorylation of integrin alpha5 and interaction of integrin alpha5 with epidermal growth factor receptor (EGFR), leading to EGFR tyrosine phosphorylation at tyrosine residues Tyr-845 and Tyr-1173. Tyrosine epidermal growth factor receptor Rattus norvegicus
3 We found that prothrombin treatment of rat hepatocytes without addition of any growth factor induced tyrosine phosphorylation of integrin alpha5 and interaction of integrin alpha5 with epidermal growth factor receptor (EGFR), leading to EGFR tyrosine phosphorylation at tyrosine residues Tyr-845 and Tyr-1173. Tyrosine epidermal growth factor receptor Rattus norvegicus
4 We found that prothrombin treatment of rat hepatocytes without addition of any growth factor induced tyrosine phosphorylation of integrin alpha5 and interaction of integrin alpha5 with epidermal growth factor receptor (EGFR), leading to EGFR tyrosine phosphorylation at tyrosine residues Tyr-845 and Tyr-1173. Tyrosine epidermal growth factor receptor Rattus norvegicus
5 EGFR tyrosine phosphorylation triggered phosphorylation of its down-stream target Shc and the activation of the c-Jun N-terminal kinase (JNK) pathway. Tyrosine epidermal growth factor receptor Rattus norvegicus