ArticleEMBO reports2005
Bcr is a negative regulator of the Wnt signalling pathway.
Article in EMBO reports, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 42 citations in OpenAlex.
- DDR1 contributes to kidney inflammation and fibrosis by promoting the phosphorylation of BCR and STAT3.JCI insight · 2022Article
- Collagen Kinase Receptors as Potential Therapeutic Targets in Metastatic Colon Cancer.Frontiers in oncology · 2020Review
- Inhibition of DDR1-BCR signalling by nilotinib as a new therapeutic strategy for metastatic colorectal cancer.EMBO molecular medicine · 2018Article
- Modulation of Dkk-3 and claudin-5 as new therapeutic strategy in the treatment of meningiomas.Oncotarget · 2017Article
- Roles of transcriptional factor 7 in production of inflammatory factors for lung diseases.Journal of translational medicine · 2015Review
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- Kaposi's sarcoma-associated herpesvirus microRNAs repress breakpoint cluster region protein expression, enhance Rac1 activity, and increase in vitro angiogenesis.Journal of virology · 2015Article
- An RNA-seq protocol to identify mRNA expression changes in mouse diaphyseal bone: applications in mice with bone property altering Lrp5 mutations.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2013Article
- Article
- Article
- Expression patterns of microRNAs associated with CML phases and their disease related targets.Molecular cancer · 2011Article
- Bcr-Abl-mediated redox regulation of the PI3K/AKT pathway.Leukemia · 2009Article
- BCR-ABL-transformed GMP as myeloid leukemic stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Article
- MUC1 oncoprotein regulates Bcr-Abl stability and pathogenesis in chronic myelogenous leukemia cells.Cancer research · 2007Article
- Bcr-Abl stabilizes beta-catenin in chronic myeloid leukemia through its tyrosine phosphorylation.The EMBO journal · 2007Article
- Article
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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Wnt signalling pathway can activate transcription of genes such as c-myc through beta-catenin. Here, we describe the protein breakpoint cluster region, Bcr, as a negative regulator of this pathway. Bcr can form a complex with beta-catenin and negatively regulate expression of c-Myc. Knockdown of Bcr by short interfering RNA relieves the block and activates expression of c-Myc. Expression of Bcr in the human colon carcinoma cell line HCT116, which has a high level of endogenous beta-catenin, leads to reduced c-Myc expression. The negative effect is exerted by the amino terminus of Bcr, which does not harbour the kinase domain. Bcr-Abl, the oncogene protein expressed in chronic myelogenous leukaemia (CML), does not bind to beta-catenin. It phosphorylates Bcr in the first exon sequence on tyrosines, which abrogates the binding of Bcr to beta-catenin. The inhibitor of the Bcr-Abl tyrosine kinase, STI-571 or Gleevec, a drug against CML, reverses this effect. Our data contribute to the understanding of Bcr as a tumour suppressor in the Wnt signalling pathway, as well as in CML.
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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.