ArticleMolecular biotechnology2001
Cdk pathway: cyclin-dependent kinases and cyclin-dependent kinase inhibitors.
Article in Molecular biotechnology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Synergistic Anticancer Effect of a Combination of Berbamine and Arcyriaflavin A against Glioblastoma Stem-like Cells.Molecules (Basel, Switzerland) · 2022Article
- Cyclin-dependent kinase 9 (CDK9) predicts recurrence in Middle Eastern epithelial ovarian cancer.Journal of ovarian research · 2021Article
- Pan-cancer genetic analysis identifies PARK2 as a master regulator of G1/S cyclins.Nature genetics · 2014Article
- Expression of verotoxin-1 receptor Gb3 in breast cancer tissue and verotoxin-1 signal transduction to apoptosis.BMC cancer · 2009Article
- Anoxic fibroblasts activate a replication checkpoint that is bypassed by E1a.Molecular and cellular biology · 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
2 authors.
Funding
Abstract
Many mechanisms either activate or inhibit the cdks and thereby either promote or arrest progression through the mitotic cell cycle. Since the signal transduction pathways emanating from extracellular mitogens and the agents controlling these pathways are complicated there may yet be novel mechanisms of cell cycle regulation remaining to be elucidated. In this article we outline the different techniques used to study the cell cycle and its regulation. These include: establishing that the cell cycle is arrested by propidium iodide staining followed by FACS analysis or by measuring 3H-thymidine incorporation into DNA; measuring the amount of cyclin/cdk associated kinase activity; assessing the steady-state expression profiles of cyclins, cdks and ckis by immunoblotting; and investigating the formation of complexes between these proteins by coimmunoprecipitations. Caveats and advantages of each technique are discussed. Following this paradigm yielded the discovery of the cell cycle inhibitors p27Kip1 and p21Cip1 and could very well lead to the discovery or novel cell cycle regulatory mechanisms.
Indexed as
Identifiers
11725487What 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.