Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

A dominant-negative form of the E3 ubiquitin ligase Cullin-1 disrupts the correct allocation of cell fate in the neural crest lineage.

Development (Cambridge, England) - 1 Feb 2006

Voigt Jana, Papalopulu Nancy

Abstract excerpt

Selective protein degradation is an efficient and rapid way of terminating protein activity. Defects in protein degradation are associated with a number of human diseases, including potentially DiGeorge syndrome, which is characterised by abnormal development of the neural crest lineage during embryogenesis. We describe the identification of Xenopus Cullin-1, an E3 ubiquitin ligase, and show that blocking the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cullin Proteins
Share to DiGeorge Syndrome
Share to Embryonic Development

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Ganglia

Share to Melanocytes

Share to Neural Crest

Share to Xenopus laevis

Share to Xenopus Proteins

Source

Identifiers

PMID: 16396913
DOI: 10.1242/dev.02201

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A dominant-negative form of the E3 ubiquitin ligase Cullin-1 disrupts the correct allocation of cell fate in the neural crest lineage.PMID 16396913Read ↗

Cullin-4 regulates Wingless and JNK signaling-mediated cell death in the Drosophila eye.Semantic proximity Read ↗

C. elegans CAND-1 regulates cullin neddylation, cell proliferation and morphogenesis in specific tissues.Semantic proximity Read ↗

Cullin-5 plays multiple roles in cell fate specification and synapse formation during Drosophila development.Semantic proximity Read ↗

A screen for X-linked mutations affecting Drosophila photoreceptor differentiation identifies Casein kinase 1α as an essential negative regulator of wingless signaling.Semantic proximity Read ↗

The ubiquitin ligase Nedd4 regulates craniofacial development by promoting cranial neural crest cell survival and stem-cell like properties.Semantic proximity Read ↗

cul-1 is required for cell cycle exit in C. elegans and identifies a novel gene family.Semantic proximity Read ↗

Distinct protein degradation mechanisms mediated by Cul1 and Cul3 controlling Ci stability in Drosophila eye development.Semantic proximity Read ↗

Loss of Cul1 results in early embryonic lethality and dysregulation of cyclin E.Semantic proximity Read ↗

Requirements of multiple domains of SLI-1, a Caenorhabditis elegans homologue of c-Cbl, and an inhibitory tyrosine in LET-23 in regulating vulval differentiation.Semantic proximity Read ↗

The E3 ubiquitin ligase component, Cereblon, is an evolutionarily conserved regulator of Wnt signalingSemantic proximity Read ↗

The Caenorhabditis elegans Skp1-related gene family: diverse functions in cell proliferation, morphogenesis, and meiosis.Semantic proximity Read ↗

Notch signaling in the mammalian central nervous system: insights from mouse mutants.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.