ReviewSmall GTPases2016
Meet me in the cytoplasm: A role for p27(Kip1) in the control of H-Ras.
Review in Small GTPases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 3 citations in OpenAlex.
- TFAM Loss Induces Oxidative Stress and Divergent Phenotypes in Glioblastoma Metabolic Subtypes.International journal of molecular sciences · 2025Article
- Metformin exerts multitarget antileukemia activity in JAK2Cell death & disease · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The small GTPases of the Ras family play a pivotal role in the regulation of cell proliferation and motility, both in normal and transformed cells. In particular, the 3 genes encoding for the N-, H- and K-Ras are frequently mutated in human cancer and their inappropriate regulation, expression and subcellular localization can drive tumor onset and progression. Activation of the Ras-MAPK pathway directly signals on the cell cycle machinery by regulating the expression and/or localization of 2 key cell cycle player, Cyclin D1 and p27(Kip1). We recently reported that in normal fibroblasts, following mitogenic stimuli, p27(Kip1) translocates to the cytoplasm where it regulates H-Ras localization and activity. This regulatory mechanism ensures that cells pass beyond the restriction point of the cell cycle only when the proper level of stimulation is reached. Here, we comment on this new evidence that possibly represents one of the ways that cells have developed during evolution to ensure that the cell decision to divide is taken only when time and context are appropriate.
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.