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Diane Lejeune

Researcher at Ludwig Institute for Cancer Research

Publications -  8
Citations -  1398

Diane Lejeune is an academic researcher from Ludwig Institute for Cancer Research. The author has contributed to research in topics: Interleukin-21 receptor & Glycoprotein 130. The author has an hindex of 7, co-authored 8 publications receiving 1319 citations.

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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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Cutting Edge: STAT Activation By IL-19, IL-20 and mda-7 Through IL-20 Receptor Complexes of Two Types

TL;DR: IL-10-related cytokines include IL-20 and IL-22, which induce, respectively, keratinocyte proliferation and acute phase production by hepatocytes, as well as IL-19, melanoma differentiation-associated gene 7, and AK155, three cytokines for which no activity nor receptor complex has been described thus far.
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Cloning and Characterization of IL-22 Binding Protein, a Natural Antagonist of IL-10-Related T Cell-Derived Inducible Factor/IL-22

TL;DR: A recombinant protein was found to bind IL-10-related T cell-derived inducible factor/IL-22, and to inhibit the activity of this cytokine on hepatocytes and intestinal epithelial cells, and it is proposed to name this natural cytokine antagonist IL-22BP for IL- 22 binding protein.
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Cloning of a new type II cytokine receptor activating signal transducer and activator of transcription (STAT)1, STAT2 and STAT3.

TL;DR: The identification of a new gene encoding a transmembrane protein of 520 amino acids, showing 22% amino acid identity with the extracellular domain of the interleukin (IL)-20 receptor is reported, suggesting that LICR2 is a signalling receptor for a new cytokine of the IL-10 family.
Journal Article

STAT5 activation is required for interleukin-9-dependent growth and transformation of lymphoid cells.

TL;DR: The data suggest that STAT5 is an important mediator of IL-9-driven proliferation and that dysregulation of STAT5 activation favors tumorigenesis of lymphoid cells.