ArticleMolecular and cellular biology2004
A direct binding site for Grb2 contributes to transformation and leukemogenesis by the Tel-Abl (ETV6-Abl) tyrosine kinase.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Modulation of the bone marrow microenvironment by acute B-cell lymphoblastic leukemia-derived large oncosomes.Blood advances · 2026Article
- [Myeloid/lymphoid neoplasm with ETV6::ABL1 fusion: a case report and literature review].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2025Review
- Exploitation of the fibrinolytic system by B-cell acute lymphoblastic leukemia and its therapeutic targeting.Nature communications · 2024Article
- Characteristics and literature review of ETV6::ABL1 fusion gene-positive acute myeloid leukemia.International journal of hematology · 2024Review
- The Diverse Roles of ETV6 Alterations in B-Lymphoblastic Leukemia and Other Hematopoietic Cancers.Advances in experimental medicine and biology · 2024Review
- Myeloid/lymphoid neoplasms with eosinophilia/ basophilia and ETV6-ABL1 fusion: cell-of-origin and response to tyrosine kinase inhibition.Haematologica · 2021Article
- ETV6-ABL1 fusion combined with monosomy 7 in childhood B-precursor acute lymphoblastic leukemia.International journal of hematology · 2018Article
- SHP2 is required for BCR-ABL1-induced hematologic neoplasia.Leukemia · 2018Article
- Article
- A Case of Chronic Myeloid Leukemia With Rare Variant ETV6/ABL1 Rearrangement.Annals of laboratory medicine · 2017Article
- Characterization of leukemias with ETV6-ABL1 fusion.Haematologica · 2016Article
- Germline mutations in ETV6 are associated with thrombocytopenia, red cell macrocytosis and predisposition to lymphoblastic leukemia.Nature genetics · 2015Article
- The role of RAS effectors in BCR/ABL induced chronic myelogenous leukemia.Frontiers of medicine · 2013Article
- Myeloproliferative neoplasm with ETV6-ABL1 fusion: a case report and literature review.Molecular cytogenetics · 2013Article
- GAB2--a scaffolding protein in cancer.Molecular cancer research : MCR · 2012Review
- Structure, regulation, signaling, and targeting of abl kinases in cancer.Genes & cancer · 2012Article
- Gab adapter proteins as therapeutic targets for hematologic disease.Advances in hematology · 2012Article
- Article
- Function, regulation and pathological roles of the Gab/DOS docking proteins.Cell communication and signaling : CCS · 2009Article
- Intrinsic differences between the catalytic properties of the oncogenic NUP214-ABL1 and BCR-ABL1 fusion protein kinases.Leukemia · 2008Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
A direct binding site for the Grb2 adapter protein is required for the induction of fatal chronic myeloid leukemia (CML)-like disease in mice by Bcr-Abl. Here, we demonstrate direct binding of Grb2 to the Tel-Abl (ETV6-Abl) fusion protein, the product of complex (9;12) chromosomal translocations in human leukemia, via tyrosine 314 encoded by TEL exon 5. A Tel-Abl point mutant (Y314F) and a splice variant without TEL exon 5 sequences (Deltae5) lacked Grb2 interaction and exhibited decreased binding and phosphorylation of the scaffolding protein Gab2 and impaired activation of phosphatidylinositol 3-kinase, Akt, and extracellular signal-regulated kinase/mitogen-activated protein kinase in hematopoietic cells. Tel-Abl Y314F and Deltae5 were unable to transform fibroblasts to anchorage-independent growth and were defective for B-lymphoid transformation in vitro and lymphoid leukemogenesis in vivo. Previously, we demonstrated that full-length Tel-Abl induced two distinct myeloproliferative diseases in mice: CML-like leukemia similar to that induced by Bcr-Abl and a novel syndrome of small-bowel myeloid infiltration endotoxemia and hepatic and renal failure. Lack of the Grb2 binding site had no effect on development of small bowel syndrome but significantly attenuated the induction of CML-like disease by Tel-Abl. These results suggest that direct binding of Grb2 is a common mechanism contributing to leukemogenesis by oncogenic Abl fusion proteins.
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