ArticleNature cell biology2011
A damage limitation exercise.
Article in Nature cell biology, 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.
- Mutant p53 perturbs DNA replication checkpoint control through TopBP1 and Treslin.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Epigenetic alteration to activate Bmp2-Smad signaling in Raf-induced senescence.World journal of biological chemistry · 2016Article
- Regulation of oncogene-induced cell cycle exit and senescence by chromatin modifiers.Cancer biology & therapy · 2012Review
- Global heterochromatin loss: a unifying theory of aging?Epigenetics · 2012Article
- c-Abl promotes osteoblast expansion by differentially regulating canonical and non-canonical BMP pathways and p16INK4a expression.Nature cell biology · 2012Article
- Activation of Bmp2-Smad1 signal and its regulation by coordinated alteration of H3K27 trimethylation in Ras-induced senescence.PLoS genetics · 2011Article
Corrections and comments
- Comment on
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is a potent tumour suppressor mechanism that is often accompanied by activation of dna damage response (DDR) signalling and marked heterochromatinization. Senescence-associated heterochromatin is now shown to limit DDR, thus reducing apoptosis and promoting survival of senescent cells.
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.