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

Distinct GAB2 signaling pathways are essential for myeloid and lymphoid transformation and leukemogenesis by BCR-ABL1.

Blood - 7 Apr 2016

Gu Shengqing, Chan Wayne W, Mohi Golam, Rosenbaum Joel, Sayad Azin, Lu Zhibin, Virtanen Carl, Li Shaoguang, Neel Benjamin G, Van Etten Richard A

Abstract excerpt

Tyrosine kinase inhibitors (TKIs) directed against BCR-ABL1, the product of the Philadelphia (Ph) chromosome, have revolutionized treatment of patients with chronic myeloid leukemia (CML). However, acquired resistance to TKIs is a significant clinical problem in CML, and TKI therapy is much less effective against Ph(+)B-cell acute lymphoblastic leukemia (B-ALL). BCR-ABL1, via phosphorylated Tyr177, recruits the...

Read the complete abstract on PubMed

Topics

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

Share to Cell Transformation, Neoplastic
Share to Fusion Proteins, bcr-abl

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Leukemia, Myeloid

Share to Phosphatidylinositol 3-Kinases

Share to Phosphoproteins

Share to Precursor Cell Lymphoblastic Leukemia-Lymphoma

Share to Protein Tyrosine Phosphatase, Non-Receptor Type 11

Share to Transduction, Genetic

Source

Open in PubMed Open full text

Identifiers

PMID: 26773044
DOI: 10.1182/blood-2015-06-653006
PMCID: PMC4825414

Genes

GAB2
ABL1
BCR
GRB2
SRC

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. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Distinct GAB2 signaling pathways are essential for myeloid and lymphoid transformation and leukemogenesis by BCR-ABL1.PMID 26773044Read ↗

The Grb2 binding site is required for the induction of chronic myeloid leukemia-like disease in mice by the Bcr/Abl tyrosine kinase.Semantic proximity Read ↗

GAB2 couples genetic drivers and signaling networks in acute myeloid leukemia.Semantic proximity Read ↗

Gab1 is required for EGF receptor signaling and the transformation by activated ErbB2.Semantic proximity Read ↗

G-CSF-induced tyrosine phosphorylation of Gab2 is Lyn kinase dependent and associated with enhanced Akt and differentiative, not proliferative, responses.Semantic proximity Read ↗

Molecular biology of chronic myeloid leukemia.Semantic proximity Read ↗

BCR-ABL-negative chronic myeloid leukemia.Semantic proximity Read ↗

G-CSF stimulates Jak2-dependent Gab2 phosphorylation leading to Erk1/2 activation and cell proliferation.Semantic proximity Read ↗

JAK2 is dispensable for maintenance of JAK2 mutant B-cell acute lymphoblastic leukemias.Semantic proximity Read ↗

BCR-ABL: The molecular mastermind behind chronic myeloid leukemiaSemantic proximity Read ↗

Inhibition of the Gab2/PI3K/mTOR signaling ameliorates myeloid malignancy caused by Ptpn11 (Shp2) gain-of-function mutations.Semantic proximity Read ↗

Oncogenic signaling: new insights and controversies from chronic myeloid leukemiaSemantic proximity Read ↗

The coiled-coil domain and Tyr177 of bcr are required to induce a murine chronic myelogenous leukemia-like disease by bcr/abl.Semantic proximity Read ↗

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