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Michael Cornell

Researcher at University of Manchester

Publications -  12
Citations -  4704

Michael Cornell is an academic researcher from University of Manchester. The author has contributed to research in topics: Genome & Notch signaling pathway. The author has an hindex of 12, co-authored 12 publications receiving 4490 citations. Previous affiliations of Michael Cornell include University of Maryland, Baltimore.

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Comparative assessment of large-scale data sets of protein-protein interactions.

TL;DR: Comprehensive protein–protein interaction maps promise to reveal many aspects of the complex regulatory network underlying cellular function and are compared with each other and with a reference set of previously reported protein interactions.
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Genome sequencing and analysis of the versatile cell factory Aspergillus niger CBS 513.88

Herman Jan Pel, +70 more
- 01 Feb 2007 - 
TL;DR: The filamentous fungus Aspergillus niger is widely exploited by the fermentation industry for the production of enzymes and organic acids, particularly citric acid, and the sequenced genome revealed a large number of major facilitator superfamily transporters and fungal zinc binuclear cluster transcription factors.
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Growth control of the eukaryote cell: a systems biology study in yeast

TL;DR: This work constitutes a first comprehensive systems biology study on growth-rate control in the eukaryotic cell and has direct implications for advanced studies on cell growth, in vivo regulation of metabolic fluxes for comprehensive metabolic engineering, and for the design of genome-scale systems biology models of the eUKaryoticcell.
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Regulation of notch endosomal sorting and signaling by Drosophila Nedd4 family proteins.

TL;DR: This work shows in Drosophila that Notch signaling is limited by the activity of two Nedd4 family HECT domain proteins, Suppressor of deltex [Su(dx)] and DNedd4, and proposes a model in which endocytic sorting of Notch mediates a decision between its activation and downregulation.
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The Drosophila melanogaster Suppressor of deltex gene, a regulator of the Notch receptor signaling pathway, is an E3 class ubiquitin ligase.

TL;DR: Overexpression of Su( dx) results in ectopic vein differentiation, wing margin loss, and wing growth phenotypes and enhances the phenotypes of loss-of-function mutations in Notch, evidence that supports the conclusion that Su(dx) has a role in the downregulation of Notch signaling.