ReviewScience signaling2011
Ubiquitin on ras: warden or partner in crime?
Review in Science signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- The role of ubiquitination in tumorigenesis and targeted drug discovery.Signal transduction and targeted therapy · 2020Review
- Therapeutic targeting of RAS: New hope for drugging the "undruggable".Biochimica et biophysica acta. Molecular cell research · 2020Review
- RAS GTPases are modified by SUMOylation.Oncotarget · 2018Article
- BCL-XNature communications · 2017Article
- The Significance of Ras Activity in Pancreatic Cancer Initiation.International journal of biological sciences · 2016Review
- Differences in the regulation of K-Ras and H-Ras isoforms by monoubiquitination.The Journal of biological chemistry · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Signal transduction through Ras translates extracellular signals into biological responses, including cell proliferation, cell survival, growth, and differentiation. For these reasons, dysregulating Ras can have dramatic effects at the cellular and organismal levels. Germline mutations that increase Ras signaling disrupt development, whereas mutational activation of Ras in somatic cells can cause cancer. Thus, identifying additional mechanisms that positively or negatively regulate Ras could have profound implications for treating human diseases. New evidence identifies K-Ras monoubiquitination as a previously unknown means to potentiate Ras signaling.
Indexed as
Identifiers
What OpenQuestion holds
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.