ArticleOncogene2002
Cdc6 requires anchorage for its expression.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 23 citations in OpenAlex.
- General strategy for understanding intracellular molecular interaction cascades that elicit stimulus-invoked biological processes.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2016Article
- Successive phosphorylation of p27(KIP1) protein at serine-10 and C terminus crucially controls its potency to inactivate Cdk2.The Journal of biological chemistry · 2012Article
- Cdc6 protein obstructs apoptosome assembly and consequent cell death by forming stable complexes with activated Apaf-1 molecules.The Journal of biological chemistry · 2012Article
- Rho-associated kinase connects a cell cycle-controlling anchorage signal to the mammalian target of rapamycin pathway.The Journal of biological chemistry · 2011Article
- Molecular architecture of the DNA replication origin activation checkpoint.The EMBO journal · 2010Article
- Promoter-wide analysis of Smad4 binding sites in human epithelial cells.Cancer science · 2009Article
- ATP-dependent activation of p21WAF1/CIP1-associated Cdk2 by Cdc6.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- N-acetyl-cysteine enhances growth in BCR-ABL-transformed cells.Cancer science · 2005Article
- Overexpression of Cdk6-cyclin D3 highly sensitizes cells to physical and chemical transformation.Oncogene · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblasts need anchorage to extracellular matrix to transit from G1 to S phase, but no longer after oncogenic transformation. Here we report that Cdc6 protein essential for the activation of replication origins requires anchorage or oncogenic stimulation for its execution. Upon anchorage loss, Cdc6 expression is shut off both transcriptionally and post-transcriptionally in a rat fibroblast despite enforced activation of E2F-dependent promoters. However, stimulation of this cell with oncogenic growth factors suppresses this shutoff and concurrently activates Cdk2 and Cdk6/4, thereby overriding the anchorage requirement for the G1-S transition and consequently enabling cells to perform anchorage-independent S phase entry. Analysis with enforced expression of Cdc6 indicates that the G1 cyclin-dependent kinases and Cdc6 constitute major cell cycle targets for the restriction of the G1-S transition by anchorage loss.
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.