Pub. Date : 2003 Jul 4
PMID : 12702722
5 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Neuro-2a cell binding to laminin increased endogenous FAK and p190RhoGEF tyrosine phosphorylation, and co-transfection of a dominant-negative inhibitor of FAK activity, termed FRNK, inhibited lamininstimulated p190RhoGEF tyrosine phosphorylation and p21 RhoA GTP binding. | Tyrosine | PTK2 protein tyrosine kinase 2 | Mus musculus |
| 2 | Neuro-2a cell binding to laminin increased endogenous FAK and p190RhoGEF tyrosine phosphorylation, and co-transfection of a dominant-negative inhibitor of FAK activity, termed FRNK, inhibited lamininstimulated p190RhoGEF tyrosine phosphorylation and p21 RhoA GTP binding. | Tyrosine | PTK2 protein tyrosine kinase 2 | Mus musculus |
| 3 | Overexpression of FAK in Neuro-2a cells increased both endogenous p190RhoGEF tyrosine phosphorylation and RhoA activity, whereas these events were inhibited by FRNK co-expression. | Tyrosine | PTK2 protein tyrosine kinase 2 | Mus musculus |
| 4 | Because insulin-like growth factor 1 treatment of Neuro-2a cells increased FAK tyrosine phosphorylation and enhanced p190RhoGEF-mediated activation of RhoA, our results support the conclusion that FAK association with p190RhoGEF functions as a signaling pathway downstream of integrins and growth factor receptors to stimulate Rho activity. | Tyrosine | PTK2 protein tyrosine kinase 2 | Mus musculus |
| 5 | Because insulin-like growth factor 1 treatment of Neuro-2a cells increased FAK tyrosine phosphorylation and enhanced p190RhoGEF-mediated activation of RhoA, our results support the conclusion that FAK association with p190RhoGEF functions as a signaling pathway downstream of integrins and growth factor receptors to stimulate Rho activity. | Tyrosine | PTK2 protein tyrosine kinase 2 | Mus musculus |