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Novo Nordisk is a Danish multinational pharmaceutical company headquartered in Bagsvaerd, Denmark, with production facilities in seven countries, and affiliates or offices in 75 countries.Novo Nordisk manufactures and markets pharmaceutical products and services. Key products include diabetes care medications and devices. Novo Nordisk is also involved with haemostasis management, growth hormone therapy and hormone replacement therapy. The company makes several drugs under various brand names, including Levemir, NovoLog, Novolin R, NovoSeven, NovoEight and Victoza.Novo Nordisk employs more than 40,000 people globally, and marketed its products in 180 countries. It is the largest publicly traded company in the Nordic countries by market capitalization. The corporation was created in 1989 through a merger of two Danish companies which date back to the 1920s. The Novo Nordisk logo is the Apis bull, one of the sacred animals of ancient Egypt.Novo Nordisk is a full member of the European Federation of Pharmaceutical Industries and Associations .The company was ranked 25th among 100 best companies to work for in 2010 by Fortune. In January 2012, Novo Nordisk was named as the most sustainable company in the world by the business magazine Corporate Knights while spin-off company Novozymes was named fourth. Novo Nordisk was ranked 72nd on “Fortune’s 100 Best Companies to Work For®” list within the U.S. state of New Jersey as of January 2014. Wikipedia.

The fate of cells arrested in mitosis by antimitotic compounds is complex but is influenced by competition between pathways promoting cell death and pathways promoting mitotic exit. As components of both of these pathways are regulated by Cdc20-dependent degradation, I hypothesize that variations in Cdc20 protein levels, rather than mutations in checkpoint genes, could affect cell fate during prolonged mitotic arrest. This hypothesis is supported by experiments where manipulation of Cdc20 levels affects the response to antimitotic compounds. The observed differences in Cdc20 levels between cell lines likely reflects differences in the rate of synthesis or degradation of the protein; therefore, understanding these pathways at a molecular level could pave the way for modulating the activity of Cdc20, in turn presenting novel therapeutic possibilities. © 2011 WILEY Periodicals, Inc.

Cox J.,Max Planck Institute of Biochemistry | Mann M.,Max Planck Institute of Biochemistry | Mann M.,Novo Nordisk AS
Annual Review of Biochemistry | Year: 2011

Systems biology requires comprehensive data at all molecular levels. Mass spectrometry (MS)-based proteomics has emerged as a powerful and universal method for the global measurement of proteins. In the most widespread format, it uses liquid chromatography (LC) coupled to high-resolution tandem mass spectrometry (MS/MS) to identify and quantify peptides at a large scale. This peptide intensity information is the basic quantitative proteomic data type. It is used to quantify proteins between different proteome states, including the temporal variation of the proteome, to determine the complete primary structure of proteins including posttranslational modifications, to localize proteins to organelles, and to determine protein interactions. Here, we describe the principles of analysis and the areas of biology where proteomics can make unique contributions. The large-scale nature of proteomics data and its high accuracy pose special opportunities as well as challenges in systems biology that have been largely untapped so far. © 2011 by Annual Reviews. All rights reserved.

Neelsen K.J.,University of Zurich | Neelsen K.J.,Novo Nordisk AS | Lopes M.,University of Zurich
Nature Reviews Molecular Cell Biology | Year: 2015

The remodelling of replication forks into four-way junctions following replication perturbation, known as fork reversal, was hypothesized to promote DNA damage tolerance and repair during replication. Albeit conceptually attractive, for a long time fork reversal in vivo was found only in prokaryotes and specific yeast mutants, calling its evolutionary conservation and physiological relevance into question. Based on the recent visualization of replication forks in metazoans, fork reversal has emerged as a global, reversible and regulated process, with intriguing implications for replication completion, chromosome integrity and the DNA damage response. The study of the putative in vivo roles of recently identified eukaryotic factors in fork remodelling promises to shed new light on mechanisms of genome maintenance and to provide novel attractive targets for cancer therapy. © 2015 Macmillan Publishers Limited. All rights reserved.

Tremaroli V.,Sahlgrenska University Hospital | Tremaroli V.,Gothenburg University | Backhed F.,Sahlgrenska University Hospital | Backhed F.,Gothenburg University | Backhed F.,Novo Nordisk AS
Nature | Year: 2012

The link between the microbes in the human gut and the development of obesity, cardiovascular disease and metabolic syndromes, such as type 2 diabetes, is becoming clearer. However, because of the complexity of the microbial community, the functional connections are less well understood. Studies in both mice and humans are helping to show what effect the gut microbiota has on host metabolism by improving energy yield from food and modulating dietary or the host-derived compounds that alter host metabolic pathways. Through increased knowledge of the mechanisms involved in the interactions between the microbiota and its host, we will be in a better position to develop treatments for metabolic disease. © 2012 Macmillan Publishers Limited. All rights reserved.

Frequent infusions of intravenous factor VIII (FVIII) are required to prevent bleeding associated with hemophilia A. To reduce the treatment burden, recombinant FVIII with a longer half-life was developed without changing the protein structure. FVIII-polyethylene glycol (PEG) conjugates were prepared using an enzymatic process coupling PEG (ranging from 10 to 80 kDa) selectively to a unique O-linked glycan in the FVIII B-domain. Binding to von Willebrand factor (VWF) was maintained for all conjugates. Upon cleavage by thrombin, the B-domain and the associated PEG were released, generating activated FVIII (FVIIIa) with the same primary structure and specific activity as native FVIIIa. In both FVIII- and VWF-deficient mice, the half-life was found to increase with the size of PEG. In vivo potency and efficacy of FVIII conjugated with a 40-kDa PEG (N8-GP) and unmodified FVIII were not different. N8-GP had a longer duration of effect in FVIII-deficient mouse models, approximately a twofold prolonged half-life in mice, rabbits, and cynomolgus monkeys; however, the prolongation was less pronounced in rats. Binding capacity of N8-GP on human monocyte-derived dendritic cells was reduced compared with unmodified FVIII, resulting in several-fold reduced cellular uptake. In conclusion, N8-GP has the potential to offer efficacious prevention and treatment of bleeds in hemophilia A at reduced dosing frequency.

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