نتایج جستجو برای: tnfr

تعداد نتایج: 1060  

2002
Sebastiano Miscia Marco Marchisio Alfredo Grilli Valentina Di Valerio Lucia Centurione Giuseppe Sabatino Francesco Garaci Giorgio Zauli Ezio Bonvini Angela Di Baldassarre

The biological actions of tumor necrosis factor (TNF) are mediated by two cell surface receptors, TNFR-1 and TNFR-2. These receptors do not display protein tyrosine kinase activity. Nevertheless, an early TNFinduced activation of specific tyrosine kinases has been reported as an important cue to the cellular response to this cytokine. Here we present evidence that TNFinduces the activation of t...

Journal: :The Journal of Experimental Medicine 1997
Mitsuru Matsumoto Yang-Xin Fu Hector Molina Guangming Huang Jinho Kim Dori A. Thomas Moon H. Nahm David D. Chaplin

In mice deficient in either lymphotoxin alpha (LT-alpha) or type I tumor necrosis factor receptor (TNFR-I), organized clusters of follicular dendritic cells (FDC) and germinal centers (GC) are absent from the spleen. We investigated the role of LT-alpha and TNFR-I in the establishment of spleen FDC and GC structure by using reciprocal bone marrow (BM) transfer. When LT-alpha-deficient mice were...

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 1997
J Fang Y Wang J M Krueger

Tumor necrosis factor (TNF) is a well characterized sleep-regulatory substance. To study receptor mechanisms for the sleep-promoting effects of TNF, sleep patterns were determined in control and TNF 55 kDa receptor knock-out (TNFR-KO) mice with a B6 x 129 background after intraperitoneal injections of saline or murine TNFalpha. The TNFR-KO mice had significantly less baseline sleep than the con...

Journal: :Journal of immunology 2004
Terry W Wright Gloria S Pryhuber Patricia R Chess Zhengdong Wang Robert H Notter Francis Gigliotti

CD8(+) T cells contribute to the pathophysiology of Pneumocystis pneumonia (PcP) in a murine model of AIDS-related disease. The present studies were undertaken to more precisely define the mechanisms by which these immune cells mediate the inflammatory response that leads to lung injury. Experimental mice were depleted of either CD4(+) T cells or both CD4(+) and CD8(+) T cells and then infected...

Journal: :The Journal of clinical investigation 2006
Kazuhiro Aoki Hiroaki Saito Cecile Itzstein Masaji Ishiguro Tatsuya Shibata Roland Blanque Anower Hussain Mian Mariko Takahashi Yoshifumi Suzuki Masako Yoshimatsu Akira Yamaguchi Pierre Deprez Patrick Mollat Ramachandran Murali Keiichi Ohya William C Horne Roland Baron

Activating receptor activator of NF-kappaB (RANK) and TNF receptor (TNFR) promote osteoclast differentiation. A critical ligand contact site on the TNFR is partly conserved in RANK. Surface plasmon resonance studies showed that a peptide (WP9QY) that mimics this TNFR contact site and inhibits TNF-alpha-induced activity bound to RANK ligand (RANKL). Changing a single residue predicted to play an...

Journal: :Mediators of Inflammation 2006
Sunil Kumar Raghav Bhawna Gupta Charu Agrawal Ved P. Chaturvedi Hasi R. Das

We examined the role of tumor necrosis factor (TNF-alpha) and its related signaling intermediates leading to apoptosis/proliferation in the peripheral blood mononuclear cells (PBMCs) of RA patients. The constitutive expression of mRNA for TNF-alpha receptors (TNFR-I and TNFR-II) and the adapter molecules, such as the TNF receptor-associated death domain protein (TRADD), Fas-associated death dom...

2013
Amit Kumar Wasim Abbas Georges Herbein

Tumor necrosis factor (TNF) and TNF receptors (TNFR) superfamily members are engaged in diverse cellular phenomena such as cellular proliferation, morphogenesis, apoptosis, inflammation, and immune regulation. Their role in regulating viral infections has been well documented. Viruses have evolved with numerous strategies to interfere with TNF-mediated signaling indicating the importance of TNF...

Journal: :Journal of virology 2005
S A Huber D Sartini

Giving C57BL/6 mice 10(4) PFU of coxsackievirus B3 (H3 variant) fails to induce myocarditis, but increasing the initial virus inoculum to 10(5) or 10(6) PFU causes significant cardiac disease. Virus titers in the heart were equivalent at days 3 and 7 in mice given all three virus doses, but day 3 titers in the pancreases of mice inoculated with 10(4) PFU were reduced. Tumor necrosis factor alph...

Journal: :American journal of physiology. Heart and circulatory physiology 2012
Ting C Zhao Ling Zhang Jun T Liu Tai L Guo

Transient activation of p38 through anisomycin is demonstrated to precondition the heart against myocardial injury. However, it remains unknown whether specific TNF-α receptor (TNFR) p55/p75 and Nox2, a subunit of NADPH oxidase, are involved in this event. We sought to investigate whether the genetic disruption of TNFRp55/p75 and Nox2 eliminated cardioprotection elicited by anisomycin and wheth...

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