ReviewMolecular biotechnology2006
Control of the G2/M transition.
Review in Molecular biotechnology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 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
139 citing papers in PubMed, 271 citations in OpenAlex.
- Preclinical analyses and phase I evaluation of LY2603618 administered in combination with pemetrexed and cisplatin in patients with advanced cancer.Investigational new drugs · 2014Trial
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- Two paired HPV-59 cervical cancer cell lines with distinct chemoradioresistant phenotypes.Scientific reports · 2026Article
- Crocin and eugenol enhance radiosensitivity in oral squamous cell carcinoma cells via apoptotic pathways and cell cycle regulation. Type of study: in vitro.BMC complementary medicine and therapies · 2026Article
- Pan-cancer atlas analysis of FANCB and its potential mechanism in cholangiocarcinoma.Discover oncology · 2025Article
- Cytotoxicity and cell cycle changes in prostate cancer cells with differing PSMA expression and p53 status after treatment with PSMA-targeting radioligand [Scientific reports · 2025Article
- G-quadruplex stabilization induces DNA breaks in pericentromeric repetitive DNA sequences in B lymphocytes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- The microRNA-6510 as a potential tumor suppressor in head and neck cancer.Scientific reports · 2025Article
- G2M-checkpoint related immune barrier structure and signature for prognosis and immunotherapy response in hepatocellular carcinoma: insights from spatial transcriptome and machine learning.Journal of translational medicine · 2025Article
- Transcriptome analysis reveals the anticancer effects of fenbendazole on ovarian cancer: an in vitro and in vivo study.BMC cancer · 2024Article
- HIV-1 Vif disrupts phosphatase feedback regulation at the kinetochore, leading to a pronounced pseudo-metaphase arrest.bioRxiv : the preprint server for biology · 2024Article
- Article
- Knockdown of TFAP2E results in rapid GOncology letters · 2024Article
- The enhanced cytotoxicity on breast cancer cells by Tanshinone I-induced photodynamic effect.Scientific reports · 2023Article
- Transcription factor E4F1 as a regulator of cell life and disease progression.Science advances · 2023Review
- Evaluation of Single Dose and Fractionated Dose of I-131 Radiolabeled Nanoparticles for Triple-Negative Breast Cancer Treatment.Biomedicines · 2023Article
- Article
79 more citing papers are in PubMed but not listed here.
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 2 institutions in 1 country.
Funding
Abstract
The G2 checkpoint prevents cells from entering mitosis when DNA is damaged, providing an opportunity for repair and stopping the proliferation of damaged cells. Because the G2 checkpoint helps to maintain genomic stability, it is an important focus in understanding the molecular causes of cancer. Many different methods have been used to investigate the G2 checkpoint and uncover some of the underlying mechanisms. Because cell cycle controls are highly conserved, a remarkable synergy between the genetic power of model organisms and biochemical analyses is possible and has uncovered control mechanisms that operate in many diverse species, including humans. CDC2, the cyclin-dependent kinase that normally drives cells into mitosis, is the ultimate target of pathways that mediate rapid arrest in G2 in response to DNA damage. Additional pathways ensure that the arrest is stably maintained. When mammalian cells contain damaged DNA, the p53 tumor suppressor and the Rb family of transcriptional repressors work together to downregulate a large number of genes that encode proteins required for G2 and M. Elimination of these essential cell cycle proteins helps to keep the cells arrested in G2.
Indexed as
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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.