ArticleMolecular and cellular biology1998
Raf-1 physically interacts with Rb and regulates its function: a link between mitogenic signaling and cell cycle regulation.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
61 citing papers in PubMed, 120 citations in OpenAlex.
- Systemic dual delivery of a tumor-inhibiting plasmid expressing p16 and shRaf.Biochemical and biophysical research communications · 2025Article
- The role of CRAF in cancer progression: from molecular mechanisms to precision therapies.Nature reviews. Cancer · 2024Review
- YWHAE-NUTM2 oncoprotein regulates proliferation and cyclin D1 via RAF/MAPK and Hippo pathways.Oncogenesis · 2021Article
- Adrenomedullin-CALCRL axis controls relapse-initiating drug tolerant acute myeloid leukemia cells.Nature communications · 2021Article
- LncRNA RP11-19E11 is an E2F1 target required for proliferation and survival of basal breast cancer.NPJ breast cancer · 2020Article
- Nuclear localized Raf1 isoform alters DNA-dependent protein kinase activity and the DNA damage response.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- ETS-targeted therapy: can it substitute for MEK inhibitors?Clinical and translational medicine · 2017Review
- Stimulation of β-adrenergic receptors plays a protective role via increased expression of RAF-1 and PDX-1 in hyperglycemic rat pancreatic islet (RIN-m5F) cells.Archives of medical science : AMS · 2017Article
- RRD-251 enhances all-trans retinoic acid (RA)-induced differentiation of HL-60 myeloblastic leukemia cells.Oncotarget · 2016Article
- Tank binding kinase 1 is a centrosome-associated kinase necessary for microtubule dynamics and mitosis.Nature communications · 2015Article
- Activated k-ras, but not h-ras or N-ras, regulates brain neural stem cell proliferation in a raf/rb-dependent manner.Stem cells (Dayton, Ohio) · 2015Article
- The Mammalian Cell Cycle Regulates Parvovirus Nuclear Capsid Assembly.PLoS pathogens · 2015Article
- Article
- Targeting RAS-ERK signalling in cancer: promises and challenges.Nature reviews. Drug discovery · 2014Review
- The clinical development of MEK inhibitors.Nature reviews. Clinical oncology · 2014Review
- Article
- Selective disruption of rb-raf-1 kinase interaction inhibits pancreatic adenocarcinoma growth irrespective of gemcitabine sensitivity.Molecular cancer therapeutics · 2013Article
- BRAF mutant non-small cell lung cancer and treatment with BRAF inhibitors.Translational lung cancer research · 2013Review
- Article
- Posttranslational modifications of the retinoblastoma tumor suppressor protein as determinants of function.Genes & cancer · 2012Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 3 countries.
Funding
Abstract
Cells initiate proliferation in response to growth factor stimulation, but the biochemical mechanisms linking signals received at the cell surface receptors to the cell cycle regulatory molecules are not yet clear. In this study, we show that the signaling molecule Raf-1 can physically interact with Rb and p130 proteins in vitro and in vivo and that this interaction can be detected in mammalian cells without overexpressing any component. The binding of Raf-1 to Rb occurs subsequent to mitogen stimulation, and this interaction can be detected only in proliferating cells. Raf-1 can inactivate Rb function and can reverse Rb-mediated repression of E2F1 transcription and cell proliferation efficiently. The region of Raf-1 involved in Rb binding spanned residues 1 to 28 at the N terminus, and functional inactivation of Rb required a direct interaction. Serum stimulation of quiescent human fibroblast HSF8 cells led to a partial translocation of Raf-1 into the nucleus, where it colocalized with Rb. Further, Raf-1 was able to phosphorylate Rb in vitro quite efficiently. We believe that the physical interaction of Raf-1 with Rb is a vital step in the growth factor-mediated induction of cell proliferation and that Raf-1 acts as a direct link between cell surface signaling cascades and the cell cycle machinery.
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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 OpenQuestion graph.