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Stefan N. Constantinescu

Researcher at Ludwig Institute for Cancer Research

Publications -  208
Citations -  16882

Stefan N. Constantinescu is an academic researcher from Ludwig Institute for Cancer Research. The author has contributed to research in topics: Signal transduction & Receptor. The author has an hindex of 57, co-authored 190 publications receiving 14994 citations. Previous affiliations of Stefan N. Constantinescu include Carol Davila University of Medicine and Pharmacy & University of Tennessee Health Science Center.

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A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera

TL;DR: A clonal and recurrent mutation in the JH2 pseudo-kinase domain of the Janus kinase 2 (JAK2) gene in most (> 80%) polycythaemia vera patients leads to constitutive tyrosine phosphorylation activity that promotes cytokine hypersensitivity and induces erythrocytosis in a mouse model.
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Development of Human Protein Reference Database as an Initial Platform for Approaching Systems Biology in Humans

TL;DR: The Human Protein Reference Database (HPRD) as mentioned in this paper is an object database that integrates a wealth of information relevant to the function of human proteins in health and disease, including protein-protein interactions, posttranslational modifications, enzyme/substrate relationships, disease associations, tissue expression, and subcellular localization.
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Interleukin-22 (IL-22) activates the JAK/STAT, ERK, JNK, and p38 MAP kinase pathways in a rat hepatoma cell line. Pathways that are shared with and distinct from IL-10.

TL;DR: It is found that IL-22 induces activation of JAK1 and Tyk2 but not JAK2, as well as phosphorylation of STAT1, STAT3, and STAT5 on tyrosine residues, extending the similarities between IL- 22 and IL-10.
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JAK/STAT signaling in hematological malignancies

TL;DR: The nature and respective contribution of mutations dysregulating the JAK/STAT pathway in hematological malignancies are discussed and examples in which such mutations drive the disease, contribute to the phenotype, or provide a survival and proliferative advantage are presented.