Mig-6 is a negative regulator of the epidermal growth factor receptor signal
Biological Chemistry, ISSN: 1431-6730, Vol: 382, Issue: 12, Page: 1649-1662
2001
- 133Citations
- 28Captures
- 1Mentions
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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
- Citations133
- Citation Indexes133
- 133
- CrossRef97
- Captures28
- Readers28
- 28
- Mentions1
- References1
- 1
Article Description
In contrast to signal generation and transmission, the mechanisms and molecules that negatively regulate receptor tyrosine kinase (RTK) signaling are poorly understood. Here we characterize Mig-6 as a novel negative feedback regulator of the epidermal growth factor receptor (EGFR) and potential tumor suppressor. Mig-6 was identified in a yeast two-hybrid screen with the kinase active domain of the EGFR as bait. Upon EGF stimulation Mig-6 binds to the EGFR involving a highly acidic region between amino acids 985-995. This interaction is kinase activity-dependent, but independent of tyrosine 992. Mig-6 overexpression results in reduced activation of the mitogen-activated protein kinase ERK2 in response to EGF, but not FGF or PDGF, stimulation and in enhanced receptor internalization without affecting the rate of degradation. The induction of Mig-6 mRNA expression in response to EGF, but not FGF, indicates the existence of a negative regulatory feedback loop. Consistent with these findings, a possible role as tumor suppressor is indicated by Mig-6-mediated inhibition of EGFR overexpression-induced transformation of Rat1 cells.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0035700605&origin=inward; http://dx.doi.org/10.1515/bc.2001.200; http://www.ncbi.nlm.nih.gov/pubmed/11843178; https://www.degruyter.com/view/j/bchm.2001.382.issue-12/bc.2001.200/bc.2001.200.xml; https://www.degruyter.com/view/j/bchm.2001.382.issue-12/bc.2001.200/bc.2001.200.pdf; https://www.degruyter.com/document/doi/10.1515/BC.2001.200/html; http://www.degruyter.com/view/j/bchm.2001.382.issue-12/bc.2001.200/bc.2001.200.xml
Walter de Gruyter GmbH
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