ArticleBiochimica et biophysica acta2011
Delta-like 1-Lysine613 regulates notch signaling.
Article in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- The intracellular domains of the DSL ligands Serrate and Delta provide different activities.Cell communication and signaling : CCS · 2025Article
- Article
- Ubiquitinations in the notch signaling pathway.International journal of molecular sciences · 2013Article
- Ubiquitylation of p53 by the APC/C inhibitor Trim39.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Lysine-specific demethylase 1 expression in zebrafish during the early stages of neuronal development.Neural regeneration research · 2012Article
- Endocytosis and control of Notch signaling.Current opinion in cell biology · 2012Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Delta ligands are important for regulating Notch signaling through transcellular stimulation of Notch receptors. The cytoplasmic tails of Delta ligands have multiple potential regulatory sites including several lysine residues that are putative targets for ubiquitination by the E3 ubiquitin ligases, Mind Bomb and Neuralized. To identify possible roles for specific lysine residues in the cytoplasmic tail of the Notch ligand Dll1 a mutational and functional analysis was performed. Examination of a panel of individual or clustered lysine mutants demonstrated that lysine 613 (K613) in the cytoplasmic tail of Dll1 is a key residue necessary for transcellular activation of Notch signaling. Multi-ubiquitination of the Dll1 mutant Dll1-K613R was altered compared to wild type Dll1, and the K613R mutation blocked the ability of Dll1 to interact with Notch1. Finally, mutation of K613 did not affect the stability of Dll1 or its ability to traffic to recycle to the plasma membrane, but did enhance the fraction associated with lipid rafts. Collectively these results suggest that the transcellular defect in Notch signaling attributed to residue K613 in cytoplasmic tail of Dll1 may result from altering its multi-ubiquitination and increasing its retention in lipid rafts.
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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.