ArticleMolecular and cellular biology2006
mTOR-independent translational control of the extrinsic cell death pathway by RalA.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Inhibition of c-FLIP alongside TRAIL treatment suppresses prostate cancer stem cell activity.British journal of cancer · 2026Article
- The E3 ubiquitin ligase Itch restricts antigen-driven B cell responses.The Journal of experimental medicine · 2019Article
- Roles of c-FLIP in Apoptosis, Necroptosis, and Autophagy.Journal of carcinogenesis & mutagenesis · 2013Article
- c-FLIP, a master anti-apoptotic regulator.Experimental oncology · 2012Review
- Overexpression of RalBP1 in colorectal cancer is an independent predictor of poor survival and early tumor relapse.Cancer biology & therapy · 2012Article
- Novel role of c-jun N-terminal kinase in regulating the initiation of cap-dependent translation.International journal of oncology · 2012Article
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- KSR1 is overexpressed in endometrial carcinoma and regulates proliferation and TRAIL-induced apoptosis by modulating FLIP levels.The American journal of pathology · 2011Article
- RalA function in dermal fibroblasts is required for the progression of squamous cell carcinoma of the skin.Cancer research · 2011Article
- Rlip76 transports sunitinib and sorafenib and mediates drug resistance in kidney cancer.International journal of cancer · 2010Article
- Article
- A novel PTEN-dependent link to ubiquitination controls FLIPS stability and TRAIL sensitivity in glioblastoma multiforme.Cancer research · 2009Article
- RLIP76: a target for kidney cancer therapy.Cancer research · 2009Article
- Enhanced killing of androgen-independent prostate cancer cells using inositol hexakisphosphate in combination with proteasome inhibitors.British journal of cancer · 2008Article
- Cellular FLICE-like inhibitory protein (C-FLIP): a novel target for cancer therapy.Current cancer drug targets · 2008Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Oncogenic potential is associated with translational regulation, and the prevailing view is that oncogenes use mTOR-dependent pathways to up-regulate the synthesis of proteins critical for transformation. In this study, we show that RalA, a key mediator of Ras transformation, is also linked to the translational machinery. At least part of this linkage, however, is independent of mTOR and acts through RalBP1 to suppress cdc42-mediated activation of S6 kinase and the translation of the antiapoptotic protein FLIP(S). This action, rather than contributing to transformation, opens a latent tumor-suppressive mechanism that can be activated by tumor necrosis factor-related apoptosis-inducing ligand. These results show that the translational machinery is linked to tumor suppression as well as cell-proliferative pathways and that the reestablishment of cell death pathways by activation of the Ral oncogenic program provides a means for selective therapeutic targeting of Ral-driven malignancies.
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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 Socratic graph.