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Marra Jai Aghajani, Tara Laurine Roberts, Tao Yang, Charles Eugenio McCafferty, Nicole J Caixeiro, Paul DeSouza and Navin Niles

:// ) 26515600 15 Rossille D Gressier M Damotte D Maucort-Boulch D Pangault C Semana G Le Gouill S Haioun C Tarte K Lamy T , et al . High level of soluble programmed cell death ligand 1 in blood impacts

Open access

Fernando Aprile-Garcia, María Antunica-Noguerol, Maia Ludmila Budziñski, Ana C Liberman and Eduardo Arzt

through different mechanisms depending on cell context. PARP1 induces the transcriptional activity of ligand-activated ER in the breast cancer cells by recluting transcriptional coactivators to ER target genes. PARP1 modulates AR–chromatin interaction in

Open access

Sofia S Pereira, Mariana P Monteiro, Sonir R Antonini and Duarte Pignatelli

fatty acid synthetase ligand (FasL)/fatty acid synthetase receptor (Fas); TNF-related apoptosis-inducing ligand (TRAIL)/death receptor 4 and 5 (DR4 and DR5) and tumor necrosis factor α (TNF-α)/tumor necrosis factor receptor 1 (TNF1-R) ( 12 , 25 , 26

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Lin Ji, Huan-Tong Wu, Xiao-Yan Qin and Rongfeng Lan

, suggesting that it may function as a trophic factor to provide neuroprotection against the oxidative-stress-induced cell death ( 112 ). For this reason, CPE is also named as neurotrophic factor-α1 (NF-α1). However, the detailed mechanisms of the CPE

Open access

N K Stepto, D Hiam, M Gibson-Helm, S Cassar, C L Harrison, S K Hutchison, A E Joham, B J Canny, A Moreno-Asso, B J Strauss, N Hatzirodos, R J Rodgers and H J Teede

-group differences ( Fig. 3 ) suggesting aberrant signalling via the TGFβ ligand signalling network, establishing a pro-fibrotic gene program. Specifically, COL1A2 and 3A1 were 2.14 fold (99% CI: 1.8, 2.4; P  = 0.001) and 2.12 fold (99% CI: 1.7, 2.4%; P  = 0

Open access

Bilal B Mughal, Jean-Baptiste Fini and Barbara A Demeneix

( 213 ). Disruption of the TH axis may partly be due to HCB’s action on the activity and expression of hepatic Dio1 and Dio2 enzymes, respectively ( 214 ). In rats, HCB has been shown to induce apoptosis in the thyroid cells, most likely due to action on