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Principles of interleukin (IL)-6-type cytokine signalling and its regulation.
- P. Heinrich, I. Behrmann, S. Haan, H. Hermanns, G. Müller-Newen, F. Schaper
- Biology, MedicineThe Biochemical journal
- 15 August 2003
This review focuses on recent progress in the understanding of the molecular mechanisms of IL-6-type cytokine signal transduction, with emphasis on the termination and modulation of the JAK/STAT signalling pathway mediated by tyrosine phosphatases, the SOCS (suppressor of cytokine signalling) feedback inhibitors and PIAS (protein inhibitor of activated STAT) proteins.
Interleukin-6-type cytokine signalling through the gp130/Jak/STAT pathway.
- P. Heinrich, I. Behrmann, G. Müller-Newen, F. Schaper, L. Graeve
- Biology, MedicineThe Biochemical journal
- 1 September 1998
Although all IL-6-type cytokines signal through the gp130/Jak/STAT pathway, the comparison of their physiological properties shows that they elicit not only similar, but also distinct, biological responses.
Activation of STAT3 by IL-6 and IL-10 in Primary Human Macrophages Is Differentially Modulated by Suppressor of Cytokine Signaling 3 1
- C. Niemand, A. Nimmesgern, +5 authors G. Müller-Newen
- Medicine, BiologyThe Journal of Immunology
- 15 March 2003
Different sensitivities of IL-10 and IL-6 signaling toward mechanisms that inhibit the Janus kinase/STAT pathway define an important mechanism that contributes to the different anti-inflammatory potencies of these two cytokines.
Mutations in CLCN2 encoding a voltage-gated chloride channel are associated with idiopathic generalized epilepsies
A gene associated with the chloride-channel gene CLCN2, which causes a loss of function of ClC-2 channels and is expected to lower the transmembrane chloride gradient essential for GABAergic inhibition, is reported.
Two distinct types of Langerhans cells populate the skin during steady state and inflammation.
The data demonstrate the presence of two types of LCs that develop through different pathways in inflammation and steady state, which transiently or stably reconstitute the LC compartment, respectively.
Loss of androgen receptor expression promotes a stem-like cell phenotype in prostate cancer through STAT3 signaling.
It is demonstrated that loss of AR expression results in STAT3 activation in prostate cancer cells, which indicates an opposing role of AR and STAT3 in prostate CSC development.
Plasticity and cross-talk of interleukin 6-type cytokines.
- C. Garbers, H. Hermanns, +4 authors J. Scheller
- Biology, MedicineCytokine & growth factor reviews
- 1 June 2012
Molecular mechanisms of inter-familiar cytokine cross-talk are reviewed which regulate dynamics and strength of IL-6 signal transduction and focus on IL- 6-type cytokine/cytokine receptor plasticity and cross- talk exemplified by the recently identified composite cytokines IL-30/IL-6R and IL-35, the first inter-Familiar IL-8/IL -12 family member.
Barttin modulates trafficking and function of ClC-K channels.
- U. Scholl, S. Hebeisen, Audrey G H Janssen, G. Müller-Newen, A. Alekov, C. Fahlke
- Biology, MedicineProceedings of the National Academy of Sciences…
- 25 July 2006
The multiple functions of barttin might be necessary for a tight adjustment of epithelial Cl(-) conductances to ensure a precise regulation of body salt content and endocochlear potential.
Identification and functional characterization of dendritic cells in the healthy murine kidney and in experimental glomerulonephritis.
- Thilo Krüger, D. Benke, +8 authors C. Kurts
- Biology, MedicineJournal of the American Society of Nephrology…
- 1 March 2004
These results are the first to identify and characterize renal CD11c(+) cells as dendritic cells as DC and to demonstrate marked changes in experimental glomerulonephritis.
Platelet Microparticles Enhance the Vasoregenerative Potential of Angiogenic Early Outgrowth Cells After Vascular Injury
Evidence is provided that PMPs can boost the potential of E OCs to restore endothelial integrity after vascular injury and major mechanisms involve the enhancement of EOC recruitment, migration, differentiation, and release of proangiogenic factors.