ArticleMolecular and cellular biology1999
The retinoblastoma protein is linked to the activation of Ras.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
The trial behind it
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
29 citing papers in PubMed, 71 citations in OpenAlex.
- Deprivation of EGFR signal causes senolysis in PDAC with CDK4/6 inhibition.Cell death and differentiation · 2026Article
- Tumor heterogeneity in retinoblastoma: a literature review.Cancer metastasis reviews · 2025Review
- Cell cycle gene alterations associate with a redistribution of mutation risk across chromosomal domains in human cancers.Nature cancer · 2024Article
- Retinoblastoma: present scenario and future challenges.Cell communication and signaling : CCS · 2023Review
- TargetingCancers · 2021Review
- Review
- Human iPS Cell-Derived Neurons Uncover the Impact of Increased Ras Signaling in Costello Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Retinoblastoma protein and MyoD function together to effect the repression of Fra-1 and in turn cyclin D1 during terminal cell cycle arrest associated with myogenesis.The Journal of biological chemistry · 2014Article
- Twists in views on RB functions in cellular signaling, metabolism and stem cells.Cancer science · 2012Review
- Article
- Racing to block tumorigenesis after pRb loss: an innocuous point mutation wins with synthetic lethality.Cell cycle (Georgetown, Tex.) · 2010Review
- The retinoblastoma gene Rb and its family member p130 suppress lung adenocarcinoma induced by oncogenic K-Ras.Oncogene · 2009Article
- Adult stem cell maintenance and tissue regeneration in the ageing context: the role for A-type lamins as intrinsic modulators of ageing in adult stem cells and their niches.Journal of anatomy · 2008Review
- A small molecule disruptor of Rb/Raf-1 interaction inhibits cell proliferation, angiogenesis, and growth of human tumor xenografts in nude mice.Cancer research · 2008Article
- Article
- pRb-dependent cyclin D3 protein stabilization is required for myogenic differentiation.Molecular and cellular biology · 2007Article
- DA-Raf1, a competent intrinsic dominant-negative antagonist of the Ras-ERK pathway, is required for myogenic differentiation.The Journal of cell biology · 2007Article
- Rb family proteins as modulators of gene expression and new aspects regarding the interaction with chromatin remodeling enzymes.Oncogene · 2006Review
- Review
- Surprising dependency for retinoblastoma protein in ras-mediated tumorigenesis.Molecular and cellular biology · 2006Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The inner membrane-bound protein Ras integrates various extracellular signals that are subsequently communicated from the cytoplasm to the nucleus via the Raf/MEK/MAPK cascade. Here we show that the retinoblastoma protein pRb, previously reported to be a nuclear target of this pathway, can in turn influence the activation state of Ras. Rb-deficient fibroblasts display elevated levels (up to 30-fold) of activated Ras during G(1). Expression of wild-type pRb or a number of pRb mutants defective in E2F regulation reverses this effect. We provide evidence that the mid-G(1) activation of Ras in Rb-deficient cells, which occurs at the level of guanine nucleotide binding, differs from that of epidermal growth factor-induced stimulation of Ras, being dependent on protein synthesis. The aberrant levels of Ras activity associated with loss of pRb may be responsible for the differentiation defects in Rb-deficient cells, because suppression of Ras activity in Rb(-/-) fibroblasts restores the transactivation function of MyoD and the expression of a late marker of skeletal muscle differentiation. These data suggest that nuclear-cytoplasmic communication between pRb and Ras is bidirectional.
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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.