| P50 | author | George Q. Daley | Q5543595 |
| | John Kuriyan | Q6243502 |
| | Nathanael Gray | Q28112823 |
| | Markus A Seeliger | Q56891944 |
| P2093 | author name string | Mohammad Azam | |
| P2860 | cites work | An allosteric mechanism for activation of the kinase domain of epidermal growth factor receptor | Q24293598 |
| | The T790M mutation in EGFR kinase causes drug resistance by increasing the affinity for ATP | Q24649549 |
| | Processing of X-ray diffraction data collected in oscillation mode | Q26778468 |
| | Structural mechanism for STI-571 inhibition of abelson tyrosine kinase | Q27627097 |
| | Structural basis for the autoinhibition of c-Abl tyrosine kinase | Q27640773 |
| | Structures of Lung Cancer-Derived EGFR Mutants and Inhibitor Complexes: Mechanism of Activation and Insights into Differential Inhibitor Sensitivity | Q27644014 |
| | c-Src binds to the cancer drug imatinib with an inactive Abl/c-Kit conformation and a distributed thermodynamic penalty | Q27644039 |
| | Three-dimensional structure of the tyrosine kinase c-Src | Q27734749 |
| | Crystal structure of the Src family tyrosine kinase Hck | Q27734750 |
| | A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome | Q27824793 |
| | EGFR mutation and resistance of non-small-cell lung cancer to gefitinib | Q27824829 |
| | Coot: model-building tools for molecular graphics | Q27860505 |
| | Likelihood-enhanced fast translation functions | Q27860634 |
| | The conformational plasticity of protein kinases | Q27860946 |
| | Refinement of macromolecular structures by the maximum-likelihood method | Q27861011 |
| | Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells | Q28277030 |
| | A Src-like inactive conformation in the abl tyrosine kinase domain | Q28469170 |
| | Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis | Q29614337 |
| | Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia | Q29615030 |
| | Protein kinases--the major drug targets of the twenty-first century? | Q29615339 |
| | Surface comparison of active and inactive protein kinases identifies a conserved activation mechanism | Q29616720 |
| | Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification | Q29618788 |
| | Activation of the Src-family tyrosine kinase Hck by SH3 domain displacement | Q30014848 |
| | A robust bulk-solvent correction and anisotropic scaling procedure | Q30080024 |
| | Genetic complementation of cytokine signaling identifies central role of kinases in hematopoietic cell proliferation | Q31029794 |
| | Transformation of an interleukin 3-dependent hematopoietic cell line by the chronic myelogenous leukemia-specific P210bcr/abl protein | Q33682660 |
| | Abl protein-tyrosine kinase inhibitor STI571 inhibits in vitro signal transduction mediated by c-kit and platelet-derived growth factor receptors | Q33918083 |
| | Analysis of the structural basis of specificity of inhibition of the Abl kinase by STI571. | Q34134516 |
| | Structure and sequence of the cellular gene homologous to the RSV src gene and the mechanism for generating the transforming virus | Q34254297 |
| | A new mutation in the KIT ATP pocket causes acquired resistance to imatinib in a gastrointestinal stromal tumor patient | Q34331384 |
| | Inhibition of KIT tyrosine kinase activity: a novel molecular approach to the treatment of KIT-positive malignancies | Q34564857 |
| | Activity of dual SRC-ABL inhibitors highlights the role of BCR/ABL kinase dynamics in drug resistance | Q34695008 |
| | Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib | Q35071103 |
| | Variation on an Src-like theme | Q35091110 |
| | Phosphorylation of the ATP-binding loop directs oncogenicity of drug-resistant BCR-ABL mutants | Q35221149 |
| | Opportunities and challenges in the development of kinase inhibitor therapy for cancer | Q35618879 |
| | Protein kinase inhibitors: insights into drug design from structure. | Q35697409 |
| | The gatekeeper residue controls autoactivation of ERK2 via a pathway of intramolecular connectivity | Q35722118 |
| | Targeted cancer therapy | Q35953128 |
| | Strategies to overcome resistance to targeted protein kinase inhibitors | Q35968384 |
| | The P190, P210, and P230 forms of the BCR/ABL oncogene induce a similar chronic myeloid leukemia-like syndrome in mice but have different lymphoid leukemogenic activity | Q36368162 |
| | Anticipating clinical resistance to target-directed agents : the BCR-ABL paradigm | Q36466443 |
| | Abelson virus abrogation of interleukin-3 dependence in a lymphoid cell line | Q36900679 |
| | The TEL/platelet-derived growth factor beta receptor (PDGF beta R) fusion in chronic myelomonocytic leukemia is a transforming protein that self-associates and activates PDGF beta R kinase-dependent signaling pathways | Q37054452 |
| | In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutants | Q40414595 |
| | PKC412 overcomes resistance to imatinib in a murine model of FIP1L1-PDGFRα-induced myeloproliferative disease. | Q40643306 |
| | A myristoyl/phosphotyrosine switch regulates c-Abl | Q40661872 |
| | Amino acid substitutions sufficient to convert the nontransforming p60c-src protein to a transforming protein | Q40667798 |
| | Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of BCR-ABL. | Q44373949 |
| | Switching on kinases: oncogenic activation of BRAF and the PDGFR family | Q45041454 |
| | A tail of two src's: mutatis mutandis | Q45248634 |
| | Epidermal growth factor-independent transformation of Ba/F3 cells with cancer-derived epidermal growth factor receptor mutants induces gefitinib-sensitive cell cycle progression | Q46735221 |
| | A general strategy for creating "inactive-conformation" abl inhibitors | Q46748983 |
| | Inherited susceptibility to lung cancer may be associated with the T790M drug resistance mutation in EGFR. | Q46782213 |
| | Flt3 mutations from patients with acute myeloid leukemia induce transformation of 32D cells mediated by the Ras and STAT5 pathways. | Q53403767 |
| | Kinase domain mutations of BCR-ABL frequently precede imatinib-based therapy and give rise to relapse in patients with de novo Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL) | Q58023972 |
| | A molecular gate which controls unnatural ATP analogue recognition by the tyrosine kinase v-Src | Q77452190 |
| P433 | issue | 10 | |
| P407 | language of work or name | English | Q1860 |
| P921 | main subject | structural biology | Q908902 |
| P304 | page(s) | 1109-18 | |
| P577 | publication date | 2008-10-01 | |
| P1433 | published in | Nature Structural & Molecular Biology | Q1071739 |
| P1476 | title | Activation of tyrosine kinases by mutation of the gatekeeper threonine | |
| P478 | volume | 15 | |