ArticleThe EMBO journal1996
The cytostatic function of c-Abl is controlled by multiple nuclear localization signals and requires the p53 and Rb tumor suppressor gene products.
Article in The EMBO journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
72 citing papers in PubMed, 200 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
- The FABD domain is critical for the oncogenicity of BCR/ABL in chronic myeloid leukaemia.Cell communication and signaling : CCS · 2024Article
- ABL1 kinase as a tumor suppressor in AML1-ETO and NUP98-PMX1 leukemias.Blood cancer journal · 2023Article
- c-Abl Activation Linked to Autophagy-Lysosomal Dysfunction Contributes to Neurological Impairment in Niemann-Pick Type A Disease.Frontiers in cell and developmental biology · 2022Article
- Parkinson's Disease Modification Through Abl Kinase Inhibition: An Opportunity.Movement disorders : official journal of the Movement Disorder Society · 2022Review
- Role of the ABL tyrosine kinases in the epithelial-mesenchymal transition and the metastatic cascade.Cell communication and signaling : CCS · 2021Review
- Nuclear-cytoplasmic Shuttling in Chronic Myeloid Leukemia: Implications in Leukemia Maintenance and Therapy.Cells · 2019Review
- Article
- c-Abl and Parkinson's Disease: Mechanisms and Therapeutic Potential.Journal of Parkinson's disease · 2017Article
- Phosphorylation of the Mdm2 oncoprotein by the c-Abl tyrosine kinase regulates p53 tumor suppression and the radiosensitivity of mice.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Regulation of the Mdm2-p53 signaling axis in the DNA damage response and tumorigenesis.Translational cancer research · 2016Article
- Article
- Misfolding, Aggregation, and Disordered Segments in c-Abl and p53 in Human Cancer.Frontiers in oncology · 2015Review
- The capable ABL: what is its biological function?Molecular and cellular biology · 2014Review
- Defying c-Abl signaling circuits through small allosteric compounds.Frontiers in genetics · 2014Article
- c-Abl-dependent molecular circuitry involving Smad5 and phosphatidylinositol 3-kinase regulates bone morphogenetic protein-2-induced osteogenesis.The Journal of biological chemistry · 2013Article
- Genetic disruption of Abl nuclear import reduces renal apoptosis in a mouse model of cisplatin-induced nephrotoxicity.Cell death and differentiation · 2013Article
- Article
- Preclinical and clinical studies of estrogen deprivation support the PDGF/Abl pathway as a novel therapeutic target for overcoming endocrine resistance in breast cancer.Breast cancer research : BCR · 2012Article
- Activation of abl family kinases in solid tumors.Genes & cancer · 2012Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
c-Abl is a non-receptor protein-tyrosine kinase lacking a clear physiological role. A clue to its normal function is suggested by overexpression of Abl in fibroblasts, which leads to inhibition of cell growth. This effect requires tyrosine kinase activity and the Abl C-terminus. c-Abl is localized to the cell nucleus, where it can bind DNA, and interacts with the retinoblastoma protein, a potential mediator of the growth-inhibitory effect. Nuclear localization of Abl can be directed by a pentalysine nuclear localization signal in the Abl C-terminus. Here, we have identified two additional basic motifs in the Abl C-terminus, either of which can function independently of the pentalysine signal to localize Abl to the nucleus. Using a quantitative transfection assay, we show that both c-Abl and transforming Abl proteins inhibit entry into S phase and this effect is absolutely dependent on nuclear localization. Further, we demonstrate that the Abl cytostatic effect requires both the Rb and p53 tumor suppressor gene products. These results indicate that Abl inhibits cell proliferation by interacting with central elements of the cell cycle control apparatus in the nucleus, and suggest a direct connection between p53 and Rb in this growth-inhibitory pathway.
Indexed as
Identifiers
8612582PMC450068W267927007What 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.