Please use this identifier to cite or link to this item:
https://doi.org/10.1016/j.ccr.2011.02.017
DC Field | Value | |
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dc.title | A Tight Junction-Associated Merlin-Angiomotin Complex Mediates Merlin's Regulation of Mitogenic Signaling and Tumor Suppressive Functions | |
dc.contributor.author | Yi, C. | |
dc.contributor.author | Troutman, S. | |
dc.contributor.author | Fera, D. | |
dc.contributor.author | Stemmer-Rachamimov, A. | |
dc.contributor.author | Avila, J. | |
dc.contributor.author | Christian, N. | |
dc.contributor.author | Persson, N. | |
dc.contributor.author | Shimono, A. | |
dc.contributor.author | Speicher, D. | |
dc.contributor.author | Marmorstein, R. | |
dc.contributor.author | Holmgren, L. | |
dc.contributor.author | Kissil, J. | |
dc.date.accessioned | 2014-12-12T07:47:00Z | |
dc.date.available | 2014-12-12T07:47:00Z | |
dc.date.issued | 2011-04-12 | |
dc.identifier.citation | Yi, C., Troutman, S., Fera, D., Stemmer-Rachamimov, A., Avila, J., Christian, N., Persson, N., Shimono, A., Speicher, D., Marmorstein, R., Holmgren, L., Kissil, J. (2011-04-12). A Tight Junction-Associated Merlin-Angiomotin Complex Mediates Merlin's Regulation of Mitogenic Signaling and Tumor Suppressive Functions. Cancer Cell 19 (4) : 527-540. ScholarBank@NUS Repository. https://doi.org/10.1016/j.ccr.2011.02.017 | |
dc.identifier.issn | 15356108 | |
dc.identifier.uri | http://scholarbank.nus.edu.sg/handle/10635/116205 | |
dc.description.abstract | The Merlin/. NF2 tumor suppressor restrains cell growth and tumorigenesis by controlling contact-dependent inhibition of proliferation. We have identified a tight-junction-associated protein complex comprising Merlin, Angiomotin, Patj, and Pals1. We demonstrate that Angiomotin functions downstream of Merlin and upstream of Rich1, a small GTPase Activating Protein, as a positive regulator of Rac1. Merlin, through competitive binding to Angiomotin, releases Rich1 from the Angiomotin-inhibitory complex, allowing Rich1 to inactivate Rac1, ultimately leading to attenuation of Rac1 and Ras-MAPK pathways. Patient-derived Merlin mutants show diminished binding capacities to Angiomotin and are unable to dissociate Rich1 from Angiomotin or inhibit MAPK signaling. Depletion of Angiomotin in Nf2-/- Schwann cells attenuates the Ras-MAPK signaling pathway, impedes cellular proliferation in vitro and tumorigenesis in vivo. © 2011 Elsevier Inc. | |
dc.description.uri | http://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.ccr.2011.02.017 | |
dc.source | Scopus | |
dc.type | Article | |
dc.contributor.department | CANCER SCIENCE INSTITUTE OF SINGAPORE | |
dc.description.doi | 10.1016/j.ccr.2011.02.017 | |
dc.description.sourcetitle | Cancer Cell | |
dc.description.volume | 19 | |
dc.description.issue | 4 | |
dc.description.page | 527-540 | |
dc.description.coden | CCAEC | |
dc.identifier.isiut | 000289589800012 | |
Appears in Collections: | Staff Publications |
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