Mammary tumorigenesis and metastasis caused by overexpression of insulin receptor substrate 1 (IRS-1) or IRS-2
Molecular and Cellular Biology, ISSN: 0270-7306, Vol: 26, Issue: 24, Page: 9302-9314
2006
- 145Citations
- 64Captures
- 2Mentions
Metric Options: Counts1 Year3 YearSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations145
- Citation Indexes145
- 145
- CrossRef123
- Captures64
- Readers64
- 64
- Mentions2
- References2
- Wikipedia2
Article Description
Insulin receptor substrates (IRSs) are signaling adaptors that play a major role in the metabolic and mitogenic actions of insulin and insulin-like growth factors. Reports have recently noted increased levels, or activity, of IRSs in many human cancers, and some have linked this to poor patient prognosis. We found that overexpressed IRS-1 was constitutively phosphorylated in vitro and in vivo and that transgenic mice overexpressing IRS-1 or IRS-2 in the mammary gland showed progressive mammary hyperplasia, tumorigenesis, and metastasis. Tumors showed extensive squamous differentiation, a phenotype commonly seen with activation of the canonical β-catenin signaling pathway. Consistent with this, IRSs were found to bind β-catenin in vitro and in vivo. IRS-induced tumorigenesis is unique, given that the IRSs are signaling adaptors with no intrinsic kinase activity, and this supports a growing literature indicating a role for IRSs in cancer. This study defines IRSs as oncogene proteins in vivo and provides new models to develop inhibitors against IRSs for anticancer therapy. Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=33845383714&origin=inward; http://dx.doi.org/10.1128/mcb.00260-06; http://www.ncbi.nlm.nih.gov/pubmed/17030631; https://www.tandfonline.com/doi/full/10.1128/MCB.00260-06; http://mcb.asm.org/cgi/doi/10.1128/MCB.00260-06; https://syndication.highwire.org/content/doi/10.1128/MCB.00260-06; https://dx.doi.org/10.1128/mcb.00260-06; https://journals.asm.org/doi/10.1128/MCB.00260-06
Informa UK Limited
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