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

Activation mechanisms of STAT5 by oncogenic Flt3-ITD.

Blood - 1 Jul 2007

Choudhary Chunaram, Brandts Christian, Schwable Joachim, Tickenbrock Lara, Sargin Bülent, Ueker Andrea, Böhmer Frank-D, Berdel Wolfgang E, Müller-Tidow Carsten, Serve Hubert

Abstract excerpt

Mutations in the receptor tyrosine kinase Flt3 represent a very common genetic lesion in acute myeloid leukemia (AML). Internal tandem duplication (ITD) mutations clustered in the juxtamembrane domain are the most frequent and best characterized mutations found in Flt3. Oncogenic activation of Flt3 by ITD mutations is known to activate aberrant signaling including activation of STAT5 and repression of myeloid...

Read the complete abstract on PubMed

Topics

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

Share to fms-Like Tyrosine Kinase 3
Share to Janus Kinase 2

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mice, Knockout

Share to STAT5 Transcription Factor

Share to Suppressor of Cytokine Signaling 1 Protein

Share to Suppressor of Cytokine Signaling Proteins

Share to Tandem Repeat Sequences

Share to TYK2 Kinase

Source

Identifiers

PMID: 17356133
DOI: 10.1182/blood-2006-05-024018

Genes

EBP
SOCS1

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

Activation mechanisms of STAT5 by oncogenic Flt3-ITD.PMID 17356133Read ↗

Signal transduction of oncogenic Flt3.Semantic proximity Read ↗

Roles of tyrosine 589 and 591 in STAT5 activation and transformation mediated by FLT3-ITD.Semantic proximity Read ↗

Flt3 mutations from patients with acute myeloid leukemia induce transformation of 32D cells mediated by the Ras and STAT5 pathways.Semantic proximity Read ↗

STAT signaling in the pathogenesis and treatment of myeloid malignanciesSemantic proximity Read ↗

Lineage-specific STAT5 target gene activation in hematopoietic progenitor cells predicts the FLT3(+)-mediated leukemic phenotype.Semantic proximity Read ↗

Mechanism of constitutive activation of FLT3 with internal tandem duplication in the juxtamembrane domain.Semantic proximity Read ↗

SRC is a signaling mediator in FLT3-ITD– but not in FLT3-TKD–positive AMLSemantic proximity Read ↗

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

Oncogenic STAT Transcription Factors as Targets for Cancer Therapy: Innovative Strategies and Clinical TranslationSemantic proximity Read ↗

Flt3 mutations from patients with acute myeloid leukemia induce transformation of 32D cells mediated by the Ras and STAT5 pathwaysSemantic proximity Read ↗

SOCS1 cooperates with FLT3-ITD in the development of myeloproliferative disease by promoting the escape from external cytokine controlSemantic proximity Read ↗

SYK is a critical regulator of FLT3 in acute myeloid leukemia.Semantic proximity Read ↗

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