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Sebastian M.B. Nijman

Researcher at Ludwig Institute for Cancer Research

Publications -  47
Citations -  9008

Sebastian M.B. Nijman is an academic researcher from Ludwig Institute for Cancer Research. The author has contributed to research in topics: Cancer & Gene. The author has an hindex of 28, co-authored 47 publications receiving 8283 citations. Previous affiliations of Sebastian M.B. Nijman include Austrian Academy of Sciences & Netherlands Cancer Institute.

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Epac is a Rap1 guanine-nucleotide-exchange factor directly activated by cyclic AMP

TL;DR: The cloned gene encoding a guanine-nucleotide-exchange factor (GEF) for Rap1 is named Epac, which contains a cAMP-binding site and a domain that is homologous to domains of known GEFs for Ras and Rap1 that is regulated directly by cAMP.
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A Genomic and Functional Inventory of Deubiquitinating Enzymes

TL;DR: An inventory of the deubiquitinating enzymes encoded in the human genome is presented and the literature concerning these enzymes is reviewed, with particular emphasis on their function, specificity, and the regulation of their activity.
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Loss of the cylindromatosis tumour suppressor inhibits apoptosis by activating NF-κB

TL;DR: It is reported here that inhibition of one of these enzymes, the familial cylindromatosis tumour suppressor gene (CYLD), having no known function, enhances activation of the transcription factor NF-κB, and this effect can be relieved by aspirin derivatives that inhibit NF-σB activity.
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Integrative transcriptome analysis reveals common molecular subclasses of human hepatocellular carcinoma.

TL;DR: Three robust HCC subclasses are observed, each correlated with clinical parameters such as tumor size, extent of cellular differentiation, and serum alpha-fetoprotein levels, and it is indicated that S1 reflected aberrant activation of the WNT signaling pathway, S2 was characterized by proliferation as well as MYC and AKT activation, and S3 was associated with hepatocyte differentiation.
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The Deubiquitinating Enzyme USP1 Regulates the Fanconi Anemia Pathway

TL;DR: It is proposed that USP1 deubiquitinates FANCD2 when cells exit S phase or recommence cycling after a DNA damage insult and may play a critical role in the FA pathway by recycling FAN CD2.