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Showing 1–12 of 12 results

Advanced filters: Author: Gerhard Müller-Newen Clear advanced filters

Erratum: Oncostatin M drives intestinal inflammation and predicts response to tumor necrosis factor–neutralizing therapy in patients with inflammatory bowel disease

Nathaniel R West
Ahmed N Hegazy
Fiona Powrie
Amendments and Corrections06 Jun 2017
Nature Medicine

Volume: 23, P: 788
Retraction Note: Mutations in CLCN2 encoding a voltage-gated chloride channel are associated with idiopathic generalized epilepsies

Karsten Haug
Maike Warnstedt
Armin Heils
Amendments and Corrections01 Sept 2009
Nature Genetics

Volume: 41, P: 1043
Oncostatin M drives intestinal inflammation and predicts response to tumor necrosis factor–neutralizing therapy in patients with inflammatory bowel disease

The cytokine oncostatin M drives intestinal inflammation in mice, and its abundance in the intestine of patients with inflammatory bowel disease predicts response to tumor necrosis factor–neutralizing therapy.

Nathaniel R West
Ahmed N Hegazy
Fiona Powrie
Research03 Apr 2017
Nature Medicine

Volume: 23, P: 579-589
Bow to your partner for signaling

A recent study on the signaling conformation of the common receptor for the interleukin-6 family of cytokines, gp130, provides new insights into the activation mechanism of the 'tall' cytokine receptors.

Heike M Hermanns
Gerhard Müller-Newen
Serge Haan
News & Views01 Jun 2005
Nature Structural & Molecular Biology

Volume: 12, P: 476-478
CLCN2 variants in idiopathic generalized epilepsy

Ailing Kleefuß-Lie
Waltraut Friedl
Holger Lerche
Correspondence01 Sept 2009
Nature Genetics

Volume: 41, P: 954-955
Stem cell persistence in CML is mediated by extrinsically activated JAK1-STAT3 signaling

Maja Kim Kuepper
Marlena Bütow
Mirle Schemionek
Research06 Mar 2019
Leukemia

Volume: 33, P: 1964-1977
Intramolecular hydrophobic interactions are critical mediators of STAT5 dimerization

Dirk Fahrenkamp
Jinyu Li
Gerhard Müller-Newen
ResearchOpen Access18 Oct 2016
Scientific Reports

Volume: 6, P: 1-15
Anti-interleukin-6 therapy through application of a monogenic protein inhibitor via gene delivery

Dieter Görtz
Gerald S. Braun
Gerhard Müller-Newen
ResearchOpen Access01 Oct 2015
Scientific Reports

Volume: 5, P: 1-14
Mutations in CLCN2 encoding a voltage-gated chloride channel are associated with idiopathic generalized epilepsies

Karsten Haug
Maike Warnstedt
Armin Heils
Research03 Mar 2003
Nature Genetics

Volume: 33, P: 527-532
Oncostatin M regulates hematopoietic stem cell (HSC) niches in the bone marrow to restrict HSC mobilization

Kavita Bisht
Crystal McGirr
Jean-Pierre Lévesque
Research13 Sept 2021
Leukemia

Volume: 36, P: 333-347
JAK2V617F but not CALR mutations confer increased molecular responses to interferon-α via JAK1/STAT1 activation

Julia Czech
Sabrina Cordua
Steffen Koschmieder
Research23 Nov 2018
Leukemia

Volume: 33, P: 995-1010
Nucleolar-nucleoplasmic shuttling of TARG1 and its control by DNA damage-induced poly-ADP-ribosylation and by nucleolar transcription

Mareike Bütepage
Christian Preisinger
Bernhard Lüscher
ResearchOpen Access30 Apr 2018
Scientific Reports

Volume: 8, P: 1-17

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Erratum: Oncostatin M drives intestinal inflammation and predicts response to tumor necrosis factor–neutralizing therapy in patients with inflammatory bowel disease

Retraction Note: Mutations in CLCN2 encoding a voltage-gated chloride channel are associated with idiopathic generalized epilepsies

Oncostatin M drives intestinal inflammation and predicts response to tumor necrosis factor–neutralizing therapy in patients with inflammatory bowel disease

Bow to your partner for signaling

CLCN2 variants in idiopathic generalized epilepsy

Stem cell persistence in CML is mediated by extrinsically activated JAK1-STAT3 signaling

Intramolecular hydrophobic interactions are critical mediators of STAT5 dimerization

Anti-interleukin-6 therapy through application of a monogenic protein inhibitor via gene delivery

Mutations in CLCN2 encoding a voltage-gated chloride channel are associated with idiopathic generalized epilepsies

Oncostatin M regulates hematopoietic stem cell (HSC) niches in the bone marrow to restrict HSC mobilization

JAK2V617F but not CALR mutations confer increased molecular responses to interferon-α via JAK1/STAT1 activation

Nucleolar-nucleoplasmic shuttling of TARG1 and its control by DNA damage-induced poly-ADP-ribosylation and by nucleolar transcription

Search

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