Affiliation: Harvard University
- Identification of novel gene expression targets for the Ras association domain family 1 (RASSF1A) tumor suppressor gene in non-small cell lung cancer and neuroblastomaAngelo Agathanggelou
Section of Medical and Molecular Genetics, Division of Reproductive and Child Health, University of Birmingham, Birmingham B15 2TT, United Kingdom
Cancer Res 63:5344-51. 2003..The identified targets are involved in diverse cellular processes; this should help toward understanding mechanisms that contribute to RASSF1A biological activity...
- Identification of the E1A-regulated transcription factor p120 E4F as an interacting partner of the RASSF1A candidate tumor suppressor geneSarah L Fenton
Section of Medical and Molecular Genetics, Department of Reproductive and Child Health, University of Birmingham, The Medical School, Edgbaston, Birmingham, United Kingdom
Cancer Res 64:102-7. 2004..As p120(E4F) has been reported previously to interact with p14ARF, retinoblastoma, and p53, these findings provide an important link between the function of RASSF1A and other major human tumor suppressor genes...
- The tumor suppressor RASSF1A and MAP-1 link death receptor signaling to Bax conformational change and cell deathShairaz Baksh
Cancer Biology Program, Division of Hematology and Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, 1038 NRB, 330 Brookline Avenue, Boston, Massachusetts 02215, USA
Mol Cell 18:637-50. 2005..Our findings identify RASSF1A and MAP-1 as important components between death receptors and the apoptotic machinery and reveal a potential link between tumor suppression and death receptor signaling...
- Dynamics of RASSF1A/MOAP-1 association with death receptorsCaitlin J Foley
Division of Experimental Oncology, Cross Cancer Institute, Edmonton, Alberta, Canada
Mol Cell Biol 28:4520-35. 2008..The association of RASSF1A and MOAP-1 with death receptors involves an ordered recruitment to receptor complexes to promote cell death and inhibit tumor formation...
- Interleukin-3 (IL-3)-induced c-fos activation is modulated by Gab2-calcineurin interactionSaiju Pyarajan
Cancer Institute, NYU School of Medicine, New York University, New York, NY 10016, USA
J Biol Chem 283:23505-9. 2008..Furthermore Cn dephosphorylates Gab2, resulting in c-fos activation and cell proliferation. We also report that there is a direct interaction between Cn and Gab2 upon IL-3 stimulation, and Akt can regulate this interaction...