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

Differential signaling of Flt3 activating mutations in acute myeloid leukemia: a working model.

Protein & cell - 1 Feb 2011

Chan Perry M

Abstract excerpt

Receptor tyrosine kinases couple a wide variety of extracellular cues to cellular responses. The class III subfamily comprises the platelet-derived growth factor receptor, c-Kit, Flt3 and c-Fms, all of which relay cell proliferation signals upon ligand binding. Accordingly, mutations in these proteins that confer ligand-independent activation are found in a subset of cancers. These mutations cluster in the...

Read the complete abstract on PubMed

Topics

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

Share to Acute Myeloid Leukemia Research
Share to Cell Membrane
Share to fms-Like Tyrosine Kinase 3

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Leukemia, Myeloid, Acute

Share to Models, Biological

Share to Mutation

Share to Protein Structure, Tertiary

Share to Signal Transduction

Source

Open in PubMed Open full text

Identifiers

PMID: 21359601
DOI: 10.1007/s13238-011-1020-7
PMCID: PMC4875257

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Differential signaling of Flt3 activating mutations in acute myeloid leukemia: a working model.PMID 21359601Read ↗

Downstream molecular pathways of FLT3 in the pathogenesis of acute myeloid leukemia: biology and therapeutic implications.Semantic proximity Read ↗

Advances in the pathogenesis of FLT3 -mutated acute myeloid leukemia and targeted treatments.Semantic proximity Read ↗

The molecular mechanisms behind activation of FLT3 in acute myeloid leukemia and resistance to therapy by selective inhibitors.Semantic proximity Read ↗

“FLipping” the Story: FLT3-Mutated Acute Myeloid Leukemia and the Evolving Role of FLT3 InhibitorsSemantic proximity Read ↗

FLT3-ITD and its current role in acute myeloid leukaemia.Semantic proximity Read ↗

Current knowledge about FLT3 gene mutations, exploring the isoforms, and protein importance in AML.Semantic proximity Read ↗

FLT3 Mutations in Acute Myeloid Leukemia: Unraveling the Molecular Mechanisms and Implications for Targeted TherapiesSemantic proximity Read ↗

Normal and oncogenic FLT3.Semantic proximity Read ↗

Targeting Oncogenic Signaling in Mutant FLT3 Acute Myeloid Leukemia: The Path to Least ResistanceSemantic proximity Read ↗

Structural and functional alterations of FLT3 in acute myeloid leukemia.Semantic proximity Read ↗

The structural basis for autoinhibition of FLT3 by the juxtamembrane domain.Semantic proximity Read ↗

Targeting FLT3 mutations in AML: review of current knowledge and evidenceSemantic proximity Read ↗

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