Query author contributions in Reactome
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Details on Person Non-covalent (reversible) tyrosine kinase inhibitors (TKIs),...
| Class:Id | Summation:1236389 |
|---|---|
| _displayName | Non-covalent (reversible) tyrosine kinase inhibitors (TKIs),... |
| _timestamp | 2011-11-22 05:28:40 |
| created | [InstanceEdit:1236388] Orlic-Milacic, Marija, 2011-03-25 |
| modified | [InstanceEdit:1247616] Orlic-Milacic, Marija, 2011-04-04 [InstanceEdit:1660492] Orlic-Milacic, Marija, 2011-10-13 [InstanceEdit:1660602] Orlic-Milacic, Marija, 2011-10-13 [InstanceEdit:2008188] Orlic-Milacic, Marija, 2011-11-22 [InstanceEdit:2010568] Orlic-Milacic, Marija, 2011-11-22 |
| text | Non-covalent (reversible) tyrosine kinase inhibitors (TKIs), erlotinib, gefitinib, lapatinib and vandetanib, selectively inhibit EGFR-stimulated tumor cell growth by blocking EGFR mutant autophosphorylation through competitive inhibition of ATP binding to the kinase domain. A number of EGFR kinase domain mutants and extracellular domain point mutants show increased senistivity to non-covalent TKIs compared with the wild-type EGFR. EGFR kinase domain mutants may be resistant to non-covalent TKIs due to primary or secondary mutations in the kinase domain that increase the affinity of the kinase domain for ATP, such as small insertions within exon 20, and substituion of threonine 790 with methionine (T790M). |
| (summation) | [Reaction:1220610] Non-covalent tyrosine kinase inhibitors bind and inactivate sensitive ligand-responsive EGFR cancer mutants [Homo sapiens] |
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No pathways have been reviewed or authored by Non-covalent (reversible) tyrosine kinase inhibitors (TKIs),... (1236389)
