ArticleMolecular and cellular biology2002
Inactivation of NF-kappaB-dependent cell survival, a novel mechanism for the proapoptotic function of c-Abl.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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
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Who cites it
23 citing papers in PubMed, 57 citations in OpenAlex.
- FBXL8 Stabilizes IκBα and Negatively Regulated NF-κB Activation to Suppress Pancreatic Cancer Progression.International journal of biological sciences · 2026Article
- Molecular mechanism of IKK catalytic dimer docking to NF-κB substrates.Nature communications · 2024Article
- Are off-target effects of imatinib the key to improving beta-cell function in diabetes?Upsala journal of medical sciences · 2022Review
- Genotoxicity-Stimulated and CYLD-Driven Malignant Transformation.Cancer management and research · 2022Article
- c-Abl kinase regulates cell proliferation and ionizing radiation-induced G2/M arrest via phosphorylation of FHL2.FEBS open bio · 2021Article
- Post-translational Modifications of IκBα: The State of the Art.Frontiers in cell and developmental biology · 2020Review
- Activation of NF-κB in B cell receptor signaling through Bruton's tyrosine kinase-dependent phosphorylation of IκB-α.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Global Regulation of Differential Gene Expression by c-Abl/Arg Oncogenic Kinases.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- Redox-regulated pathway of tyrosine phosphorylation underlies NF-κB induction by an atypical pathway independent of the 26S proteasome.Biomolecules · 2015Article
- Sphingosine-1-phosphate mediates a reciprocal signaling pathway between stellate cells and cancer cells that promotes pancreatic cancer growth.The American journal of pathology · 2014Article
- Doxorubicin induces atypical NF-κB activation through c-Abl kinase activity in breast cancer cells.Journal of cancer research and clinical oncology · 2013Article
- Growth inhibitory effect of dihydroartemisinin on Bcr/Abl+ chronic myeloid leukemia K562 cells involve AKT, ERK and NF-κB modulation.Journal of cancer research and clinical oncology · 2012Article
- STI571 reduces TRAIL-induced apoptosis in colon cancer cells: c-Abl activation by the death receptor leads to stress kinase-dependent cell death.Journal of biomedical science · 2012Article
- PTPN13/PTPL1: an important regulator of tumor aggressiveness.Anti-cancer agents in medicinal chemistry · 2011Review
- Phosphorylation by the c-Abl protein tyrosine kinase inhibits parkin's ubiquitination and protective function.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Abelson virus transformation prevents TRAIL expression by inhibiting FoxO3a and NF-kappaB.Molecules and cells · 2010Article
- NF-kappaB activity is constitutively elevated in c-Abl null fibroblasts.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- PTPL1: a large phosphatase with a split personality.Cancer metastasis reviews · 2008Review
- Article
- Reduced tumor growth in vivo and increased c-Abl activity in PC3 prostate cancer cells overexpressing the Shb adapter protein.BMC cancer · 2007Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Using a system that expresses a constitutively kinase-active c-Abl protein [c-Abl(KA)], we identified the protein IkappaBalpha as a novel substrate of c-Abl. This kinase-substrate relationship is not only confirmed at the level of endogenous proteins but is also supported by a physical interaction between the two proteins. Interestingly, the association of c-Abl with IkappaBalpha, which is detectable in the form of nonphosphorylated proteins, is remarkably enhanced by an inducible binding of tyrosine-phosphorylated IkappaBalpha to the c-Abl SH2 domain. In contrast to the serine 32/34 phosphorylation that triggers ubiquitination and degradation of IkappaBalpha, c-Abl-mediated phosphorylation at tyrosine 305 is associated with an increase of the IkappaBalpha protein stability. Significantly, this activity is not shared by the oncogenic Bcr-Abl, because it is unique to the nuclear c-Abl. We also demonstrate that c-Abl targets the nuclear subpopulation of IkappaBalpha for phosphorylation and induces it to accumulate in the nucleus. As a consequence, NF-kappaB transcription activity is abolished, leading to an increased cellular sensitivity to the induction of apoptosis. The functional importance of c-Abl-mediated IkappaBalpha phosphorylation is highlighted by a loss of response of the IkappaBalpha(Y305F) protein to c-Abl-mediated regulation. Using cells expressing the c-Abl(KA) protein under the control of an inducible promoter, we demonstrate inactivation of the NF-kappaB-dependent cell survival pathway as one of the mechanisms for c-Abl-mediated apoptosis.
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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.