ArticleDevelopmental cell2006
An intrinsic cell cycle checkpoint pathway mediated by MEK and ERK in Drosophila.
Article in Developmental cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 22 citations in OpenAlex.
- Normal cell cycle progression requires negative regulation of E2F1 by Groucho during S phase and its relief at G2 phase.Development (Cambridge, England) · 2023Article
- Enhancing CHK1 inhibitor lethality in glioblastoma.Cancer biology & therapy · 2012Article
- The yeast mitogen-activated protein kinase Slt2 is involved in the cellular response to genotoxic stress.Cell division · 2012Article
- Article
- ARF triggers cell G1 arrest by a P53 independent ERK pathway.Molecular and cellular biochemistry · 2011Article
- CHK1 inhibitors in combination chemotherapy: thinking beyond the cell cycle.Molecular interventions · 2011Review
- Article
- Unphosphorylated STAT and heterochromatin protect genome stability.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- Extracellular signal-regulated kinases modulate DNA damage response - a contributing factor to using MEK inhibitors in cancer therapy.Current medicinal chemistry · 2011Review
- Viral oncolysis that targets Raf-1 signaling control of nuclear transport.Journal of virology · 2010Article
- Article
- The candidate MAP kinase phosphorylation substrate DPL-1 (DP) promotes expression of the MAP kinase phosphatase LIP-1 in C. elegans germ cells.Developmental biology · 2008Article
- Four-dimensional dynamics of MAPK information processing systems.Wiley interdisciplinary reviews. Systems biology and medicineReview
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 1 institution in 1 country.
Funding
Abstract
Cell cycle checkpoints are surveillance mechanisms that safeguard genome integrity. While the extrinsic pathways that halt the cell cycle in response to DNA damages have been well documented, the intrinsic pathways that ensure orderly progression of cell cycle events are not well understood. We demonstrate that Drosophila MEK and ERK constitute an essential intrinsic checkpoint pathway that restrains cell cycle progression in the absence of DNA damage and also responds to ionizing radiation to arrest the cell cycle. Embryos lacking MEK exhibit faster and extra division cycles and fail to undergo timely midblastula transition (MBT) or arrest following ionizing radiation. Conversely, constitutively activated MEK causes cell cycle arrest. Further, MEK activation in the early embryo is cell cycle-dependent and Raf independent and increases in response to ionizing radiation or in the absence of Chk1. Thus, MEK/ERK activation is required for multiple checkpoints and is essential for orderly cell cycle progression.
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.