ArticleOncogene2000
Notch(ic)-ER chimeras display hormone-dependent transformation, nuclear accumulation, phosphorylation and CBF1 activation.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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Who cites it
21 citing papers in PubMed, 44 citations in OpenAlex.
- Sex hormone receptor signaling networks drive pancreatic solid-pseudopapillary neoplasm pathogenesis and therapy.Discover oncology · 2025Review
- NOTCH1 Aberrations in Chronic Lymphocytic Leukemia.Frontiers in oncology · 2018Review
- C-terminal deletion of NOTCH1 intracellular domain (N1Scientific reports · 2017Article
- Constitutive phosphorylation of the active Notch1 intracellular domain in chronic lymphocytic leukemia cells with NOTCH1 mutation.Leukemia · 2015Article
- Gamma secretase inhibitor enhances sensitivity to doxorubicin in MDA-MB-231 cells.International journal of clinical and experimental pathology · 2015Article
- NUMB inhibition of NOTCH signalling as a therapeutic target in prostate cancer.Nature reviews. Urology · 2014Review
- Noncanonical NOTCH signaling limits self-renewal of human epithelial and induced pluripotent stem cells through ROCK activation.Molecular and cellular biology · 2013Article
- BAK activation is necessary and sufficient to drive ceramide synthase-dependent ceramide accumulation following inhibition of BCL2-like proteins.The Biochemical journal · 2013Article
- Chrysin activates Notch1 signaling and suppresses tumor growth of anaplastic thyroid carcinoma in vitro and in vivo.Cancer · 2013Article
- Notch activation stimulates migration of breast cancer cells and promotes tumor growth.Breast cancer research : BCR · 2013Article
- Article
- Loss of transcription factor KLF5 in the context of p53 ablation drives invasive progression of human squamous cell cancer.Cancer research · 2011Article
- Hierarchical phosphorylation within the ankyrin repeat domain defines a phosphoregulatory loop that regulates Notch transcriptional activity.The Journal of biological chemistry · 2011Article
- GSK3beta is a negative regulator of the transcriptional coactivator MAML1.Nucleic acids research · 2009Article
- The prolyl-isomerase Pin1 is a Notch1 target that enhances Notch1 activation in cancer.Nature cell biology · 2009Article
- ErbB2 induces Notch1 activity and function in breast cancer cells.Clinical and translational science · 2008Article
- It's T-ALL about Notch.Oncogene · 2008Review
- Notch activation induces endothelial cell cycle arrest and participates in contact inhibition: role of p21Cip1 repression.Molecular and cellular biology · 2004Article
- Notch signaling as a therapeutic target in cancer: a new approach to the development of cell fate modifying agents.Oncogene · 2003Review
- Characterization of a high-molecular-weight Notch complex in the nucleus of Notch(ic)-transformed RKE cells and in a human T-cell leukemia cell line.Molecular and cellular biology · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Notch genes encode a family of evolutionarily conserved transmembrane receptors that are involved in many distinct cellular processes such as differentiation, proliferation and apoptosis. Notch function has been shown to be required both during development and in adult life. Moreover, several studies on spontaneous human tumors and in experimental models demonstrate that three of the four mammalian Notch genes can act as oncogenes. The mechanism by which Notch proteins induce neoplastic transformation is not known. In order to determine the early signaling events mediated by Notch during cellular transformation we constructed several inducible alleles of Notch(ic) by fusing portions of Nic to the hormone-binding domain of the estrogen receptor. Here we show that Notch(ic)-ER chimeras are conditionally activated by 4-Hydroxytamoxifen (OHT) in a dose-dependent manner. Clonal RKE cell lines expressing Notch(ic)-ER chimeras display hormone-dependent transformation in vitro. Transformation mediated by Notch(ic)-ER is reversible and chronic stimulation is necessary for the maintenance of the transformed phenotype. In response to hormone activation Notch(ic)-ER chimeras become hyperphosphorylated and accumulate in the nucleus of the cell; indicating that both phosphorylation and nuclear localization are required for Notch transforming activity.
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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.