Pages that link to "Q34134516"
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The following pages link to Analysis of the structural basis of specificity of inhibition of the Abl kinase by STI571. (Q34134516):
Displaying 50 items.
- Resistance to tyrosine kinase inhibition therapy for chronic myelogenous leukemia: a clinical perspective and emerging treatment options (Q27028181) (← links)
- Activation of tyrosine kinases by mutation of the gatekeeper threonine (Q27652166) (← links)
- Synaptic clustering of PSD-95 is regulated by c-Abl through tyrosine phosphorylation (Q28581044) (← links)
- Biology-driven cancer drug development: back to the future (Q33552888) (← links)
- A non-ATP-competitive inhibitor of BCR-ABL overrides imatinib resistance (Q33767209) (← links)
- Characteristics and outcomes of patients with chronic myeloid leukemia and T315I mutation following failure of imatinib mesylate therapy (Q33844041) (← links)
- Label-free detection of small-molecule-protein interactions by using nanowire nanosensors (Q33849527) (← links)
- Practical advice for determining the role of BCR-ABL mutations in guiding tyrosine kinase inhibitor therapy in patients with chronic myeloid leukemia (Q33878636) (← links)
- Nilotinib for the treatment of chronic myeloid leukemia: An evidence-based review (Q34130343) (← links)
- Molecular mechanisms of resistance to imatinib in Philadelphia-chromosome-positive leukaemias. (Q34175760) (← links)
- Development and targeted use of nilotinib in chronic myeloid leukemia. (Q34613968) (← links)
- Second generation inhibitors of BCR-ABL for the treatment of imatinib-resistant chronic myeloid leukaemia (Q34622576) (← links)
- Inhibition of the Bcr-Abl tyrosine kinase as a therapeutic strategy for CML. (Q35022505) (← links)
- Emerging cancer-targeted therapies (Q35064126) (← links)
- Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib (Q35071103) (← links)
- Abelson family tyrosine kinases regulate the function of nicotinic acetylcholine receptors and nicotinic synapses on autonomic neurons. (Q35080488) (← links)
- High affinity molecules disrupting GRB2 protein complexes as a therapeutic strategy for chronic myelogenous leukaemia (Q35104353) (← links)
- Resistance of Philadelphia-chromosome positive leukemia towards the kinase inhibitor imatinib (STI571, Glivec): a targeted oncoprotein strikes back (Q35128883) (← links)
- The BCR-ABL35INS insertion/truncation mutant is kinase-inactive and does not contribute to tyrosine kinase inhibitor resistance in chronic myeloid leukemia (Q35553592) (← links)
- Imatinib therapy in chronic myelogenous leukemia: strategies to avoid and overcome resistance (Q35816396) (← links)
- Synergistic interactions between imatinib mesylate and the novel phosphoinositide-dependent kinase-1 inhibitor OSU-03012 in overcoming imatinib mesylate resistance (Q35847734) (← links)
- Imatinib as a paradigm of targeted therapies (Q35870613) (← links)
- Personalized medical treatment strategies for patients with chronic myeloid leukemia (Q36118424) (← links)
- Advances in the treatment for haematological malignancies (Q36429723) (← links)
- Absence of SKP2 expression attenuates BCR-ABL-induced myeloproliferative disease (Q36843762) (← links)
- Imatinib mesylate in the treatment of hematologic malignancies (Q36960525) (← links)
- Somatic pharmacogenomics in cancer (Q37235024) (← links)
- Abl tyrosine kinase inhibitors for overriding Bcr-Abl/T315I: from the second to third generation (Q37256808) (← links)
- Unleashing the power of inhibitors of oncogenic kinases through BH3 mimetics (Q37431491) (← links)
- Molecular techniques for the personalised management of patients with chronic myeloid leukaemia (Q37696776) (← links)
- Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy (Q38361603) (← links)
- BCR: a new target in resistance mediated by BCR/ABL-315I? (Q38710583) (← links)
- Combination of panobinostat with ponatinib synergistically overcomes imatinib-resistant CML cells (Q38771802) (← links)
- Choosing the best second-line tyrosine kinase inhibitor in imatinib-resistant chronic myeloid leukemia patients harboring Bcr-Abl kinase domain mutations: how reliable is the IC₅₀? (Q39516382) (← links)
- c-Abl activates p38 MAPK independently of its tyrosine kinase activity: Implications in cisplatin-based therapy. (Q40076507) (← links)
- Endoplasmic reticulum stress initiates apoptotic death induced by STI571 inhibition of p210 bcr-abl tyrosine kinase (Q40610971) (← links)
- Ultra-deep sequencing leads to earlier and more sensitive detection of the tyrosine kinase inhibitor resistance mutation T315I in chronic myeloid leukemia (Q40973173) (← links)
- BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia (Q41980844) (← links)
- The Bcr-Abl mutations T315I and Y253H do not confer a growth advantage in the absence of imatinib. (Q42805035) (← links)
- Associations between imatinib resistance conferring mutations and Philadelphia positive clonal cytogenetic evolution in CML. (Q42979550) (← links)
- Quantifying signal changes in nano-wire based biosensors (Q43428492) (← links)
- Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of BCR-ABL. (Q44373949) (← links)
- Imatinib produces significantly superior molecular responses compared to interferon alfa plus cytarabine in patients with newly diagnosed chronic myeloid leukemia in chronic phase (Q44605528) (← links)
- Detection of ABL kinase domain mutations with denaturing high-performance liquid chromatography (Q44770281) (← links)
- Abl inhibitor BMS354825 binding mode in Abelson kinase revealed by molecular docking studies (Q46461403) (← links)
- An amino-acid switch in the BCR-ABL kinase domain modifies sensitivity to imatinib mesylate (Q46562415) (← links)
- A single nucleotide polymorphism in the coding region of ABL and its effects on sensitivity to imatinib (Q46693870) (← links)
- Molecular basis explanation for imatinib resistance of BCR-ABL due to T315I and P-loop mutations from molecular dynamics simulations (Q46703844) (← links)
- The presence of a BCR-ABL mutant allele in CML does not always explain clinical resistance to imatinib (Q46935674) (← links)
- MPT0B002, a novel microtubule inhibitor, downregulates T315I mutant Bcr-Abl and induces apoptosis of imatinib-resistant chronic myeloid leukemia cells (Q51083278) (← links)