ReviewDevelopmental biology2018
A quantitative model of developmental RTK signaling.
Review in Developmental biology, 2018. 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
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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
11 citing papers in PubMed, 18 citations in OpenAlex.
- ERK synchronizes embryonic cleavages in Drosophila.Developmental cell · 2024Article
- Finishing the egg.Genetics · 2024Article
- Article
- Capicua is a fast-acting transcriptional brake.Current biology : CB · 2021Article
- Novel synthetic biology approaches for developmental systems.Stem cell reports · 2021Review
- Molecular mechanisms underlying cellular effects of human MEK1 mutations.Molecular biology of the cell · 2021Article
- Optogenetic Rescue of a Patterning Mutant.Current biology : CB · 2020Article
- Rapid Dynamics of Signal-Dependent Transcriptional Repression by Capicua.Developmental cell · 2020Article
- Receptor Tyrosine Kinases in Development: Insights fromInternational journal of molecular sciences · 2019Review
- Optimizing photoswitchable MEK.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- The trigger (and the restriction) of Torso RTK activation.Open biology · 2018Review
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
Receptor tyrosine kinases (RTKs) control a wide range of developmental processes, from the first stages of embryogenesis to postnatal growth and neurocognitive development in the adult. A significant share of our knowledge about RTKs comes from genetic screens in model organisms, which provided numerous examples demonstrating how specific cell fates and morphologies are abolished when RTK activation is either abrogated or significantly reduced. Aberrant activation of such pathways has also been recognized in many forms of cancer. More recently, studies of human developmental syndromes established that excessive activation of RTKs and their downstream signaling effectors, most notably the Ras signaling pathway, can also lead to structural and functional defects. Given that both insufficient and excessive pathway activation can lead to abnormalities, mechanistic analysis of developmental RTK signaling must address quantitative questions about its regulation and function. Patterning events controlled by the RTK Torso in the early Drosophila embryo are well-suited for this purpose. This mini review summarizes current state of knowledge about Torso-dependent Ras activation and discusses its potential to serve as a quantitative model for studying the general principles of Ras signaling in development and disease.
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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.