ArticleProceedings of the National Academy of Sciences of the United States of America1998
Protein tyrosine phosphatase PTP1B suppresses p210 bcr-abl-induced transformation of rat-1 fibroblasts and promotes differentiation of K562 cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
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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
28 citing papers in PubMed, 103 citations in OpenAlex.
- Evaluation of Cas13d as a tool for genetic interaction mapping.Nature communications · 2025Article
- Article
- Recent advances in PTP1B signaling in metabolism and cancer.Bioscience reports · 2021Review
- Current Views on the Interplay between Tyrosine Kinases and Phosphatases in Chronic Myeloid Leukemia.Cancers · 2021Review
- Review
- KIBRA attains oncogenic activity by repressing RASSF1A.British journal of cancer · 2017Article
- Protein tyrosine phosphatase 1B targets PITX1/p120RasGAP thus showing therapeutic potential in colorectal carcinoma.Scientific reports · 2016Article
- Early endosomal escape of a cyclic cell-penetrating peptide allows effective cytosolic cargo delivery.Biochemistry · 2014Article
- Activation of abl family kinases in solid tumors.Genes & cancer · 2012Article
- Inhibition of protein-tyrosine phosphatase 1B (PTP1B) mediates ubiquitination and degradation of Bcr-Abl protein.The Journal of biological chemistry · 2011Article
- Identification of new substrates of the protein-tyrosine phosphatase PTP1B by Bayesian integration of proteome evidence.The Journal of biological chemistry · 2011Article
- PTP1B: a double agent in metabolism and oncogenesis.Trends in biochemical sciences · 2010Review
- Synergy between proteasome inhibitors and imatinib mesylate in chronic myeloid leukemia.PloS one · 2009Article
- Activation of Src by protein tyrosine phosphatase 1B Is required for ErbB2 transformation of human breast epithelial cells.Cancer research · 2009Article
- PTPROt inactivates the oncogenic fusion protein BCR/ABL and suppresses transformation of K562 cells.The Journal of biological chemistry · 2009Article
- Highly parallel identification of essential genes in cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Protein tyrosine phosphatase, PTP1B, expression and activity in rat corneal endothelial cells.Molecular vision · 2007Article
- ReSETting PP2A tumour suppressor activity in blast crisis and imatinib-resistant chronic myelogenous leukaemia.British journal of cancer · 2006Review
- Protein tyrosine phosphatase 1B negatively regulates macrophage development through CSF-1 signaling.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Reduced tumorigenicity of murine leukemia cells expressing protein-tyrosine phosphatase, PTPepsilon C.Oncogene · 2003Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The bcr-abl chimeric oncoprotein exhibits deregulated protein tyrosine kinase activity and is implicated in the pathogenesis of Philadelphia chromosome (Ph)-positive human leukemias, such as chronic myelogenous leukemia (CML). Recently we have shown that the levels of the protein tyrosine phosphatase PTP1B are enhanced in p210 bcr-abl-expressing cell lines. Furthermore, PTP1B recognizes p210 bcr-abl as a substrate, disrupts the formation of a p210 bcr-abl/Grb2 complex, and inhibits signaling events initiated by this oncoprotein PTK. In this report, we have examined whether PTP1B effects transformation induced by p210 bcr-abl. We demonstrate that expression of either wild-type PTP1B or the substrate-trapping mutant form of the enzyme (PTP1B-D181A) in p210 bcr-abl-transformed Rat-1 fibroblasts diminished the ability of these cells to form colonies in soft agar, to grow in reduced serum, and to form tumors in nude mice. In contrast, TCPTP, the closest relative of PTP1B, did not effect p210 bcr-abl-induced transformation. Furthermore, neither PTP1B nor TCPTP inhibited transformation induced by v-Abl. In addition, overexpression of PTP1B or treatment with CGP57148, a small molecule inhibitor of p210 bcr-abl, induced erythroid differentiation of K562 cells, a CML cell line derived from a patient in blast crisis. These data suggest that PTP1B is a selective, endogenous inhibitor of p210 bcr-abl and is likely to be important in the pathogenesis of CML.
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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.