|1.||Tsutsumi, Yasuo: 10 articles (02/2015 - 01/2008)|
|2.||Meldrum, Daniel R: 10 articles (09/2010 - 07/2006)|
|3.||Yoshioka, Yasuo: 9 articles (02/2015 - 01/2008)|
|4.||Kamada, Haruhiko: 8 articles (02/2015 - 01/2008)|
|5.||Mukai, Yohei: 8 articles (02/2015 - 01/2008)|
|6.||Abe, Yasuhiro: 8 articles (02/2015 - 01/2008)|
|7.||Tsunoda, Shin-ichi: 8 articles (02/2013 - 01/2008)|
|8.||Nakagawa, Shinsaku: 8 articles (02/2013 - 01/2008)|
|9.||Wang, Meijing: 8 articles (06/2010 - 07/2006)|
|10.||Nomura, Tetsuya: 7 articles (01/2011 - 01/2008)|
08/01/2013 - "In addition, a significant reduction in apoptosis of alveolar macrophages was observed in TNFR1(-/-) mice at day 3 after bacillus Calmette-Guérin infection. "
12/01/2011 - "In contrast, infection with carriage isolates lead to prolonged activation of NF-κB that was associated with a transient activation of JNK increased TACE/ADAM17-mediated shedding of TNFR1 and protection against apoptosis. "
11/15/2009 - "Here, we directly demonstrate using wild-type TNF(-/-) and TNFR1(-/-) mice that TNF does play a role in protection against vaccinia virus (VV) infection in naive mice. "
01/01/2005 - "Fas and TNFR1, but not cytolytic granule-dependent mechanisms, mediate clearance of murine liver adenoviral infection."
09/01/2000 - "In this study, we explored the regulation of protective immunity by TNFR1 and -2. In primary pulmonary infection, both TNFR1-/- and -2-/- mice manifested a high mortality after infection with H. "
06/01/2013 - "We found that autophagy is responsible for clearance of wild-type TNFR1, but when TNFR1 is mutated, the autophagy process is defective, probably accounting for mutant TNFR1 accumulation as well as TRAPS-associated induction of NF-κB activity and excessive IL-1β secretion, leading to chronic inflammation. "
10/01/2009 - "In conclusion, our study demonstrates that pharmacological and genetic inhibition of the TNF/TNFR1 binding reduce the degree of macrophages inflammation caused by LPS/IFN-gamma stimulation."
12/01/2015 - "These findings indicated that the N-glycosylation of TNFR1 played an important role during microglia activation in CNS inflammation. "
12/01/2015 - "The N-glycosylation of TNFR1 could facilitate its capability of binding to TNFα and further promote the formation of TNFα autocrine loop in microglia stimulated by TNFα, resulting in excessive microglia activation and CNS inflammation. "
12/01/2015 - "We conclude that NIK not only contributes to lymphoid organogenesis, inflammation and cell survival but also to TNFR1/RIP1-dependent cell death independently of the alternative NF-κB pathway. "
09/30/2008 - "Previous studies have shown that females have improved myocardial functional recovery, TNFR1 signaling resistance, and increased SOCS3 expression after acute ischemia/reperfusion when compared with males. "
12/01/2013 - "Taken together, this study indicated that regulation of the TNF-α/TNFR1 and JNK signal pathways may provide a new therapy for cerebral damage induced by ischemia and reperfusion. "
06/01/2010 - "Before ischemia, 1 mL of vehicle or 1 x 10(6) MSCs/mL from WT1, WT2, TNFR1KO, TNFR2KO, or TNFR1/2KO was infused into the hearts (n = 4-6 per group). "
09/01/2008 - "Recovery from ischemia was greater in TIA-1(-/-) and was diminished in TNFR1(-/-). "
11/15/2006 - "TNFR1 mediates liver injury after ischemia/reperfusion but is also mitogenic during hepatic regeneration. "
12/01/2015 - "Tumor cell membranes in both CR1 induction and control groups were positive for TNFR1 expression; however, total protein levels did not differ between the two groups. "
09/22/2015 - "Drug treatments targeting CTGF, TNFR1, and IκB signaling each prohibited the EMT and tumor progression. "
08/28/2015 - "Tag7 (PGLYRP1) in Complex with Hsp70 Induces Alternative Cytotoxic Processes in Tumor Cells via TNFR1 Receptor."
01/01/2015 - "Together our data is the first to identify a tumor promoting role of endogenous Timp3 in vivo, the spatial and temporal windows of this effect, and its dependence on Tnfr1. "
01/01/2015 - "The tumor suppression in Timp3 null mice requires Tnfr1, but does not result in alterations in the local immune compartment. "
|5.||Demyelinating Diseases (Demyelinating Disease)
02/01/1999 - "Severity of symptoms and demyelination in MOG-induced EAE depends on TNFR1."
10/01/2000 - "Studies with knockout mice in which genes of the TNF ligand/receptor superfamily are not expressed and studies with transgenic mice overexpressing TNF and TNFR reveal the critical role of the TNFR1 signalling pathway in the control of CNS demyelination and inflammation. "
10/01/2000 - "TNFR1 signalling is critical for the development of demyelination and the limitation of T-cell responses during immune-mediated CNS disease."
05/01/2011 - "Insomuch as TNFR1 mediates demyelination and TNFR2 remyelination, it could be hypothesized that anti-TNF-α agents which selectively inhibit sTNF or signals from TNFR1 could be effective in treating MS."
12/15/2009 - "CONCLUSION.: Our results suggested that the proportion of apoptotic oligodendrocytes, causing spongy axonal degeneration and demyelination, correlated with the magnitude of cord compression and that overexpression of TNF-alpha, TNFR1, and TNFR2 seems to participate in apoptosis of such cells in the chronically compressed spinal cord."
|1.||Type II Tumor Necrosis Factor Receptors
|2.||Tumor Necrosis Factor Receptors (Tumor Necrosis Factor Receptor)
|3.||Tumor Necrosis Factor-alpha (Tumor Necrosis Factor)
|4.||NF-kappa B (NF-kB)
|5.||Interleukin-1 (Interleukin 1)
|6.||Small Interfering RNA (siRNA)
|9.||Protein Kinases (Protein Kinase)
|4.||Transplantation (Transplant Recipients)
|5.||Bone Marrow Transplantation (Transplantation, Bone Marrow)