Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Paradoxical activation of c-Src as a drug-resistant mechanism.

Cell reports - 23 Mar 2021

Higuchi Makio, Ishiyama Kenichi, Maruoka Masahiro, Kanamori Ryosuke, Takaori-Kondo Akifumi, Watanabe Naoki

Abstract excerpt

ATP-competitive inhibitors have been developed as promising anti-cancer agents. However, drug-resistance frequently occurs, and the underlying mechanisms are not fully understood. Here, we show that the activation of c-Src and its downstream phosphorylation cascade can be paradoxically induced by Src-targeted and RTK-targeted kinase inhibitors. We reveal that inhibitor binding induces a conformational change in...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Dasatinib
Share to Focal Adhesion Protein-Tyrosine Kinases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Focal Adhesions

Share to GRB2 Adaptor Protein

Share to MCF-7 Cells

Share to src-Family Kinases

Share to src Homology Domains

Share to Xenopus

Source

Identifiers

PMID: 33761359
DOI: 10.1016/j.celrep.2021.108876

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Paradoxical activation of c-Src as a drug-resistant mechanism.PMID 33761359Read ↗

Profiling of the drug resistance of thousands of Src tyrosine kinase mutants uncovers a regulatory network that couples autoinhibition to catalytic domain dynamicsSemantic proximity Read ↗

Mechanisms of acquired resistance to tyrosine kinase inhibitorsSemantic proximity Read ↗

Resistance to tyrosine kinase inhibitors: calling on extra forces.Semantic proximity Read ↗

Strategies to overcome resistance to targeted protein kinase inhibitors in the treatment of cancer.Semantic proximity Read ↗

Capitalizing on paradoxical activation of the mitogen-activated protein kinase pathway for treatment of Imatinib-resistant mast cell leukemia.Semantic proximity Read ↗

Paradox-Breaking RAF Inhibitors that Also Target SRC Are Effective in Drug-Resistant BRAF Mutant MelanomaSemantic proximity Read ↗

Constitutive Cell Proliferation Regulating Inhibitor of Protein Phosphatase 2A (CIP2A) Mediates Drug Resistance to Erlotinib in an EGFR Activating Mutated NSCLC Cell Line.Semantic proximity Read ↗

Src inhibitors act through different mechanisms in Non-Small Cell Lung Cancer models depending on EGFR and RAS mutational status.Semantic proximity Read ↗

The Mitogen-Activated Protein Kinase Pathway Facilitates Resistance to the Src Inhibitor Dasatinib in Thyroid Cancer.Semantic proximity Read ↗

JC-010a, a novel selective SHP2 allosteric inhibitor, overcomes RTK/non-RTK-mediated drug resistance in multiple oncogene-addicted cancers.Semantic proximity Read ↗

Biochemical Mechanisms of Resistance to Small-Molecule Protein Kinase InhibitorsSemantic proximity Read ↗

Molecular Understanding of the Acquisition of Resistance to Anti-cancer Drugs Associated with the Exacerbation of Cancer.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.