ArticleJournal of controlled release : official journal of the Controlled Release Society2009
Controlling subcellular localization to alter function: Sending oncogenic Bcr-Abl to the nucleus causes apoptosis.
Article in Journal of controlled release : official journal of the Controlled Release Society, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- The Coiled Coil and C2 Domains Modulate BCR Localization and BCR-ABL1 Compartmentalization, Transforming Activity and TKI Responsiveness.International journal of molecular sciences · 2025Article
- Effect of HSP90AB1 and CC domain interaction on Bcr-Abl protein cytoplasm localization and function in chronic myeloid leukemia cells.Cell communication and signaling : CCS · 2021Article
- Alterations in the nucleocytoplasmic transport in apoptosis: Caspases lead the way.Cell proliferation · 2018Review
- RETRACTED: Blockade of Y177 and Nuclear Translocation of Bcr-Abl Inhibits Proliferation and Promotes Apoptosis in Chronic Myeloid Leukemia Cells.International journal of molecular sciences · 2017Article
- Nuclear PI3K signaling in cell growth and tumorigenesis.Frontiers in cell and developmental biology · 2015Review
- Article
- The DNA binding domain of p53 is sufficient to trigger a potent apoptotic response at the mitochondria.Molecular pharmaceutics · 2013Article
- A chimeric p53 evades mutant p53 transdominant inhibition in cancer cells.Molecular pharmaceutics · 2013Article
- Controlled access of p53 to the nucleus regulates its proteasomal degradation by MDM2.Molecular pharmaceutics · 2013Article
- Utilizing the estrogen receptor ligand-binding domain for controlled protein translocation to the insoluble fraction.Pharmaceutical research · 2012Article
- Enhanced and selective killing of chronic myelogenous leukemia cells with an engineered BCR-ABL binding protein and imatinib.Molecular pharmaceutics · 2012Article
- Selective targeting of c-Abl via a cryptic mitochondrial targeting signal activated by cellular redox status in leukemic and breast cancer cells.Pharmaceutical research · 2012Article
- Direct induction of apoptosis using an optimal mitochondrially targeted p53.Molecular pharmaceutics · 2012Article
- Changing the subcellular location of the oncoprotein Bcr-Abl using rationally designed capture motifs.Pharmaceutical research · 2012Article
- Improved coiled-coil design enhances interaction with Bcr-Abl and induces apoptosis.Molecular pharmaceutics · 2012Article
- Disruption of Bcr-Abl coiled coil oligomerization by design.The Journal of biological chemistry · 2011Article
- Controlling subcellular delivery to optimize therapeutic effect.Therapeutic delivery · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Altering the subcellular localization of signal transducing proteins is a novel approach for therapeutic intervention. Mislocalization of tumor suppressors, oncogenes, or factors involved in apoptosis results in aberrant functioning of these proteins, leading to disease. In the case of chronic myelogenous leukemia (CML), cytoplasmic Bcr-Abl causes oncogenesis/proliferation. On the other hand, nuclear entrapment of endogenous Bcr-Abl (in K562 human leukemia cells) causes apoptosis. The goal of this study was to determine whether ectopically expressed Bcr-Abl could cause apoptosis of K562 cells when specifically directed to the nucleus via strong nuclear localization signals (NLSs). A single NLS from SV40 large T-antigen or four NLSs were subcloned to Bcr-Abl (1NLS-Bcr-Abl or 4NLS-Bcr-Abl). When transfected into K562 cells, only 4NLS-Bcr-Abl translocated to the nucleus. Bcr-Abl alone was found to localize in the cell cytoplasm, colocalizing with actin due to its actin binding domain. 1NLS-Bcr-Abl also localized with actin. Apoptosis induced by 4NLS-Bcr-Abl was evaluated 24h post-transfection by morphologic determination, DNA staining, and caspase-3 assay. This is the first demonstration that altering the location of ectopically expressed Bcr-Abl can kill leukemia cells. Multiple NLSs are required to overcome Bcr-Abl binding to actin, thus driving it into the nucleus and causing apoptosis.
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What OpenQuestion holds
Registered trials
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.