ArticleOncogene2001
Accumulation of high levels of the p53 and p130 growth-suppressing proteins in cell lines stably over-expressing cyclin-dependent kinase 6 (cdk6).
Article in Oncogene, 2001. 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
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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.
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, 20 citations in OpenAlex.
- CDKs Functional Analysis in Low Proliferating Early-Stage Pancreatic Ductal Adenocarcinoma.Journal of bioinformatics and systems biology : Open access · 2023Article
- IFITM3 knockdown reduces the expression of CCND1 and CDK4 and suppresses the growth of oral squamous cell carcinoma cells.Cellular oncology (Dordrecht, Netherlands) · 2019Article
- Proteotranscriptomic Measurements of E6-Associated Protein (E6AP) Targets in DU145 Prostate Cancer Cells.Molecular & cellular proteomics : MCP · 2018Article
- A New Way to Treat Brain Tumors: Targeting Proteins Coded by Microcephaly Genes?: Brain tumors and microcephaly arise from opposing derangements regulating progenitor growth. Drivers of microcephaly could be attractive brain tumor targets.BioEssays : news and reviews in molecular, cellular and developmental biology · 2018Review
- Targeting CDK6 in cancer: State of the art and new insights.Cell cycle (Georgetown, Tex.) · 2015Review
- Article
- The other side of the coin: the tumor-suppressive aspect of oncogenes and the oncogenic aspect of tumor-suppressive genes, such as those along the CCND-CDK4/6-RB axis.Cell cycle (Georgetown, Tex.) · 2014Review
- Unexpected reduction of skin tumorigenesis on expression of cyclin-dependent kinase 6 in mouse epidermis.The American journal of pathology · 2011Article
- Parkin enhances the expression of cyclin-dependent kinase 6 and negatively regulates the proliferation of breast cancer cells.The Journal of biological chemistry · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Cyclin-dependent kinase 6(cdk6) is present in randomly proliferating cultures of 3T3 cells but has little detectable enzymatic activity. Significant activity is detected only during a short period in early G1 phase. To examine the possible functions of cdk6 in 3T3 cells, lines stably over-expressing cdk6 were constructed and compared to normal 3T3 cells or cell lines with reduced cdk6 levels due to expression of a dominant-negative form of the protein. Over-expression of cdk6 in cells, which led to high levels of activity even in proliferating cultures, had dramatic effects. Cell lines stably over-expressing wild-type cdk6 had a markedly reduced growth rate compared to parental 3T3 cells or lines expressing a dominant-negative form of cdk6. They also over-produced the p53 and p130 proteins and had increased sensitivity to UV-irradiation. Irradiation resulted in accumulation of the Bax protein and rapid cell death. Levels of p53 and p130 proteins were down-regulated and the growth rate of the cells was increased by introduction of the dominant-negative form of cdk6 into cells over-expressing cdk6, indicating that cdk6 is involved in the overproduction of p53 and p130. The results suggest that cdk6, through regulation of growth-suppressing molecules, may play a role in halting cellular growth when proliferation is inappropriate.
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.