ArticleScientific reports2018
Src kinase phosphorylates Notch1 to inhibit MAML binding.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 18 citations in OpenAlex.
- Notch intracellular domains form transcriptionally active heterodimeric complexes on sequence-paired sites.Scientific reports · 2024Article
- Integrins control epithelial stem cell proliferation in theFrontiers in cell and developmental biology · 2023Article
- Src family kinases, adaptor proteins and the actin cytoskeleton in epithelial-to-mesenchymal transition.Cell communication and signaling : CCS · 2021Review
- Notch-ing up knowledge on molecular mechanisms of skin fibrosis: focus on the multifaceted Notch signalling pathway.Journal of biomedical science · 2021Review
- Notch in mechanotransduction - from molecular mechanosensitivity to tissue mechanostasis.Journal of cell science · 2020Review
- Precision medicine for human cancers with Notch signaling dysregulation (Review).International journal of molecular medicine · 2020Review
- Notch family members follow stringent requirements for intracellular domain dimerization at sequence-paired sites.PloS one · 2020Article
- Decoding the PTM-switchboard of Notch.Biochimica et biophysica acta. Molecular cell research · 2019Review
- A comparison of resveratrol and other polyphenolic compounds on Notch activation and endothelial cell activity.PloS one · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Notch signaling is a form of intercellular communication which plays pivotal roles at various stages in development and disease. Previous findings have hinted that integrins and extracellular matrix may regulate Notch signaling, although a mechanistic basis for this interaction had not been identified. Here, we reveal that the regulation of Notch by integrins and extracellular matrix is carried out by Src family kinases (SFKs) working downstream of integrins. We identify a physical interaction between the SFK member, c-Src, and the Notch intracellular domain (NICD) that is enhanced by β3 integrin and the integrin binding ECM protein, MAGP2. Our results demonstrate that c-Src directly phosphorylates the NICD at specific tyrosine residues and that mutation of these phosphorylation sites increases Notch responsive transcriptional activity. Furthermore, we also find that phosphorylation of the NICD by SFKs attenuates Notch mediated transcription by decreasing recruitment of MAML to the Notch co-transcriptional complex. Finally, we also find that SFK activity decreases NICD half-life. Collectively, our results provide important mechanistic data that underlie the emerging role of Notch as a general sensor and responder to extracellular signals.
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.