Publications by authors named "Russell Neuner"

Article Synopsis
  • Canonical Wnt signaling is crucial during vertebrate gastrulation for forming the neural plate border (NPB) and is believed to play a role in specifying the neural crest (NC) lineage, though direct evidence has been limited.
  • Research reveals that the disintegrin metalloproteinase ADAM13 is necessary for Wnt activation and NC induction, while its paralog ADAM19 significantly influences Wnt activity and NC specification without affecting NPB formation.
  • ADAM19 acts nonproteolytically by interacting with ADAM13 to inhibit its degradation, and by stabilizing ADAM13, it can induce NC markers using Wnt signaling, highlighting a novel interaction between these proteases in regulating Wnt
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ADAM19 is a member of the meltrin subfamily of ADAM metalloproteases. In Xenopus, ADAM19 is present as a maternal transcript. Zygotic expression starts during gastrulation and is apparent in the dorsal blastopore lip.

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Cell adhesion molecules such as cadherins alternate their expression throughout cranial neural crest (CNC) development, yet our understanding of the role of these molecules during CNC migration remains incomplete. The "mesenchymal" cadherin-11 is expressed in the CNC during migration yet prevents migration when overexpressed in the embryo, suggesting that a defined level of cadherin-11-mediated cell adhesion is required for migration. Here we show that members of the meltrin subfamily of ADAM metalloproteases cleave the extracellular domain of cadherin-11 during CNC migration.

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The effect of methionine deprivation (methionine stress) on the proliferation, survival, resistance to chemotherapy, and regulation of gene and protein expression in pancreatic tumor lines is examined. Methionine stress prevents successful mitosis and promotes cell cycle arrest and accumulation of cells with multiple micronuclei with decondensed chromatin. Inhibition of mitosis correlates with CDK1 down-regulation and/or inhibition of its function by Tyr(15) phosphorylation or Thr(161) dephosphorylation.

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