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

BCR-ABL induces opposite phenotypes in murine ES cells according to STAT3 activation levels.

Cellular signalling - 1 Jan 2009

Coppo Paul, Dusanter-Fourt Isabelle, Vainchenker William, Turhan Ali G

Abstract excerpt

The mechanisms by which p210-BCR-ABL determines hematopoietic stem cells fate remain poorly understood. To better understand the behavior of BCR-ABL in pluripotent stem cells, we previously developed a murine embryonic stem (ES) cell model transformed by p210-BCR-ABL and reported that BCR-ABL activates STAT3, a major protein involved in ES cells self-renewal, which leads specifically to inhibition of ES cells...

Read the complete abstract on PubMed

Topics

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

Share to Embryonic Stem Cells
Share to Extracellular Signal-Regulated MAP Kinases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Flavonoids

Share to Fusion Proteins, bcr-abl

Share to Imatinib Mesylate

Share to Leukemia Inhibitory Factor

Share to Mitogen-Activated Protein Kinase 3

Share to STAT3 Transcription Factor

Source

Identifiers

PMID: 18835438
DOI: 10.1016/j.cellsig.2008.09.006

Genes

BCR
STAT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

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

BCR-ABL induces opposite phenotypes in murine ES cells according to STAT3 activation levels.PMID 18835438Read ↗

Constitutive and specific activation of STAT3 by BCR-ABL in embryonic stem cells.Semantic proximity Read ↗

MEK kinase 1 is essential for Bcr-Abl-induced STAT3 and self-renewal activity in embryonic stem cells.Semantic proximity Read ↗

Cancer-Associated STAT3 Mutations Maintain ES Cell Self-Renewal Through Phosphorylation-Independent Mechanisms.Semantic proximity Read ↗

Regulated expression of P210 Bcr-Abl during embryonic stem cell differentiation stimulates multipotential progenitor expansion and myeloid cell fateSemantic proximity Read ↗

Biological effects of T315I-mutated BCR-ABL in an embryonic stem cell-derived hematopoiesis model.Semantic proximity Read ↗

Overexpression of a dominant negative form of STAT3 selectively impairs hematopoietic stem cell activity.Semantic proximity Read ↗

Stat3 is required to maintain the full differentiation potential of mammary stem cells and the proliferative potential of mammary luminal progenitors.Semantic proximity Read ↗

Microarray analysis of LIF/Stat3 transcriptional targets in embryonic stem cells.Semantic proximity Read ↗

Progressive changes in the leukemogenic signaling in BCR/ABL-transformed cells.Semantic proximity Read ↗

<i>ABL</i> Oncogenes and Phosphoinositide 3-Kinase: Mechanism of Activation and Downstream EffectorsSemantic proximity Read ↗

SOCS2 is dispensable for BCR/ABL1-induced chronic myeloid leukemia-like disease and for normal hematopoietic stem cell functionSemantic proximity Read ↗

STAT3 positively regulates an early step in B-cell development.Semantic proximity Read ↗

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