ArticleLeukemia2008
Intrinsic differences between the catalytic properties of the oncogenic NUP214-ABL1 and BCR-ABL1 fusion protein kinases.
Article in Leukemia, 2008. 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, 49 citations in OpenAlex.
- NUP214 in Acute Myeloid Leukemia.Cells · 2025Review
- Article
- Article
- Pharmacological approaches to understanding protein kinase signaling networks.Frontiers in pharmacology · 2023Review
- SFPQ-ABL1 and BCR-ABL1 use different signaling networks to drive B-cell acute lymphoblastic leukemia.Blood advances · 2022Article
- T-Cell Acute Lymphoblastic Leukemia-Current Concepts in Molecular Biology and Management.Biomedicines · 2021Review
- A Novel ELISA-Based Peptide Biosensor Assay for Screening ABL1 ActivityFrontiers in pharmacology · 2021Article
- Case Report: The First Report ofFrontiers in oncology · 2021Article
- Cooperative Enhancer Activation by TLX1 and STAT5 Drives Development of NUP214-ABL1/TLX1-Positive T Cell Acute Lymphoblastic Leukemia.Cancer cell · 2018Article
- Alkynylnicotinamide-Based Compounds as ABL1 Inhibitors with Potent Activities against Drug-Resistant CML Harboring ABL1(T315I) Mutant Kinase.ChemMedChem · 2018Article
- Peptide Arrays: Development and Application.Analytical chemistry · 2018Review
- Aberrant Signaling Pathways in T-Cell Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2017Review
- Differential signaling networks of Bcr-Abl p210 and p190 kinases in leukemia cells defined by functional proteomics.Leukemia · 2017Article
- The genetics and molecular biology of T-ALL.Blood · 2017Review
- Unique amplification of BCR-ABL1 gene fusion in a case of T-cell acute lymphoblastic leukemia.Molecular cytogenetics · 2017Article
- Synergistic effects of selective inhibitors targeting the PI3K/AKT/mTOR pathway or NUP214-ABL1 fusion protein in human Acute Lymphoblastic Leukemia.Oncotarget · 2016Article
- NUP214-ABL1 fusion defines a rare subtype of B-cell precursor acute lymphoblastic leukemia that could benefit from tyrosine kinase inhibitors.Haematologica · 2016Article
- Article
- NUP214-ABL1-mediated cell proliferation in T-cell acute lymphoblastic leukemia is dependent on the LCK kinase and various interacting proteins.Haematologica · 2014Article
- The molecular basis of T cell acute lymphoblastic leukemia.The Journal of clinical investigation · 2012Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NUP214-ABL1 fusion kinase has recently been identified in 6% of patients with T-cell acute lymphoblastic leukemia. In contrast to the more common oncogenic ABL1 fusion BCR-ABL1, NUP214-ABL1 localizes to the nuclear pore complexes and has attenuated transforming properties in hematopoietic cells and in mouse bone marrow transplant models. We have performed a thorough biochemical comparative analysis of NUP214-ABL1 and BCR-ABL1 and show that, despite their common tyrosine kinase domain, the two fusion proteins differ in many critical catalytic properties. NUP214-ABL1 has lower in vitro tyrosine kinase activity, which is in agreement with the absence of phosphorylation on its activation loop. NUP214-ABL1 was more sensitive to imatinib (Glivec) than BCR-ABL1 in vitro and in cells, indicating a different activation state and conformation of the two ABL1 fusion kinases. Using a peptide array, we identified differences in the spectrum and efficiency of substrate peptide phosphorylation and a differential involvement of Src kinases in downstream signaling. These results clearly indicate that different fusion partners of the same kinase can determine not only localization, but also critical functional properties of the enzyme such as inhibitor sensitivity and substrate preference, with subsequent differences in downstream signaling effectors and likely consequences in disease pathogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.