ArticleCell cycle (Georgetown, Tex.)2014
MKK7 and ARF: new players in the DNA damage response scenery.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 13 citations in OpenAlex.
- Pharmacological inhibition of the MAP2K7 kinase in human disease.Frontiers in oncology · 2024Review
- Antileukemic properties of the kinase inhibitor OTSSP167 in T-cell acute lymphoblastic leukemia.Blood advances · 2023Article
- Non-Canonical Functions of the ARF Tumor Suppressor in Development and Tumorigenesis.Biomolecules · 2021Review
- Integrating the DNA damage and protein stress responses during cancer development and treatment.The Journal of pathology · 2018Review
- Article
- miR-125b inhibited epithelial-mesenchymal transition of triple-negative breast cancer by targeting MAP2K7.OncoTargets and therapy · 2016Article
- DNA damage-induced regulatory interplay between DAXX, p53, ATM kinase and Wip1 phosphatase.Cell cycle (Georgetown, Tex.) · 2015Article
- Evaluation of cytotoxicity and DNA damage response with analysis of intracellular ATM signaling pathways.Assay and drug development technologies · 2014Article
- Regulation and roles of Cdc7 kinase under replication stress.Cell cycle (Georgetown, Tex.) · 2014Review
- Systematic analysis of time-series gene expression data on tumor cell-selective apoptotic responses to HDAC inhibitors.Computational and mathematical methods in medicine · 2014Article
- ARF: a versatile DNA damage response ally at the crossroads of development and tumorigenesis.Frontiers in genetics · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 6 institutions in 7 countries.
Funding
Abstract
Sensing, integrating, and processing of stressogenic signals must be followed by accurate differential response(s) for a cell to survive and avoid malignant transformation. The DNA damage response (DDR) pathway is vital in this process, as it deals with genotoxic/oncogenic insults, having p53 as a nodal effector that performs most of the above tasks. Accumulating data reveal that other pathways are also involved in the same or similar processes, conveying also to p53. Emerging questions are if, how, and when these additional pathways communicate with the DDR axis. Two such stress response pathways, involving the MKK7 stress-activated protein kinase (SAPK) and ARF, have been shown to be interlocked with the ATM/ATR-regulated DDR axis in a highly ordered manner. This creates a new landscape in the DDR orchestrated response to genotoxic/oncogenic insults that is currently discussed.
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.