Bonvini P, Zorzi E, Basso G, Rosolen A. Bortezomib-mediated 26S proteasome inhibition causes cell-cycle arrest and induces apoptosis in CD-30+ anaplastic large cell lymphoma. Liu Y, Cell Death Dis. The novel receptor TRAIL-R4 induces NF-kappaB and protects against TRAIL-mediated apoptosis, yet retains an incomplete death domain. Its identification requires further investigations and is behind the scope of this study. Second, by showing that this induction of cytokine and chemokine expression occurs in an ERK1/2- and NFκB-dependent manner, the current study unveiled the underlying mechanisms by which TRAIL can induce an inflammatory response in human adipocytes. Immunol Today. These data demonstrate that the ERK1/2 pathway is a key player in the TRAIL-induced cytokine and chemokine expression. It turned out that 5 genes were jointly up-regulated in preadipocytes as well as in adipocytes (tumor necrosis factor alpha-induced protein 3 (TNFAIP3), chemokine C-C motif ligand 20 (CCL-20), interleukin 6 (IL-6), interleukin 8 (IL-8) and monocyte chemoattractant protein 1 (MCP-1)). Rosevear HM, Lightfoot AJ, Griffith TS. Mol Cancer Ther. CAS  Copyright © 1996-2020 , Weizmann Institute of Science. Oncogene. USA.gov. Lemke J, von Karstedt S, Zinngrebe J, Walczak H. Getting TRAIL back on track for cancer therapy. Translocation of the truncated Bid (tBID) to the mitochondria promotes the assembly of Bax-Bak oligomers and changes the permeability of the mitochondrial outer membrane. Expression profiles of circulating cytokines, chemokines and immune cells in patients with hepatitis B virus infection. Redistribution of CD95, DR4 and DR5 in rafts accounts for the synergistic toxicity of resveratrol and death receptor ligands in colon carcinoma cells. If the expression of the TRAIL molecule is increased due to the effect of IFN-γ, the infected cells get sensitized to the TRAIL molecule via HBx protein (expressed by HBV genome), which eventually leads to the apoptosis of infected cells (28). Vasc. Hengartner MO, Horvitz HR.

Nutr. While TRAIL is relatively non-toxic to normal cells, it selectively induces apoptosis in many transformed cells.
Wagner KW, Punnoose EA, Januario T, et al. TRAIL/DR5 signaling promotes macrophage foam cell formation by modulating scavenger receptor expression.

The TRAIL-mediated up-regulation of IL-8 and MCP-1 was not affected by caspase inhibition (Fig. Epub 2019 Apr 2. On day 7 of differentiation SGBS adipocytes were nucleofected with a NFκB Firefly luciferase reporter vector containing five copies of an NFκB response element that drives transcription of the Firefly luciferase reporter gene and Renilla luciferase control reporter vector using the Neon Transfection System (Thermo Fisher Scientific, Darmstadt, Germany). R.M., T.K., K.M.D. Not only are the levels of expression of TRAIL-R3 and -R4 not significantly greater than -R1 and -R2 (indeed, as noted, the expression pattern of -R3 seems to be much more restricted than those of -R1 and -R2), but the affinities of the four TRAIL receptors are actually quite similar.50,53,55, If susceptibility to the apoptosis-inducing effects of TRAIL is not controlled by “decoy” receptors, how is it controlled? Circulating levels of MCP-1 and IL-8 are elevated in human obese subjects and associated with obesity-related parameters. Of note, there was a high inter-patient variability. Hepat Mon. •  Privacy Policy   Luminescence was recorded in a Multimode Microplate Reader (Mithras LB 940, Berthold, Bad Wildbad, Germany). 2.8 A resolution crystal structure of human TRAIL, a cytokine with selective antitumor activity. Google Scholar. 2007;25(11):1390–1395. Smith CA, Farrah T, Goodwin RG. 4

Daryoush Hamidi Alamdari Schooley K, Department of Clinical Biochemistry, School of Medicine, Mashhad University of Medical Sciences, Mashhad, IR Iran, 2 Countering resistance to TRAIL-based therapeutic agents. Seki N, Hayakawa Y, Brooks AD, et al. Active caspase-8 then cleaves and activates the effector caspases directly or cleaves BID and activates the mitochondrial cell death pathway. Trautwein C, 29, 4752–4765 (2010). Herbst, R. S. et al. Griffith TS, Fialkov JM, Scott DL, et al. 39, 314–321 (2007). Tumor necrosis factor receptor superfamily members and their ligands. Polymorphism at the positions of 1525G/A and 1595C/T might influence the clearance of hepatitis B virus (HBV). Based on our findings, blocking the function of TRAIL in adipose tissue might be beneficial to either prevent or ameliorate adipose tissue inflammation. Mitsui J, Nishikawa H, Muraoka D, et al.

Osteoprotegerin (OPG) is a soluble receptor that binds TRAIL and inhibits its activity. Wyllie AH, Kerr JF, Currie AR. Article  Li J, Yin Q, Wu H. Structural basis of signal transduction in the TNF receptor superfamily. In the broadest sense, there are two means by which cell death can occur that are defined by classical biochemical and morphological criteria.1–3 One mechanism of cell death, “necrosis”, is typically induced by injury or a traumatic event, leading to the inability to maintain cell-membrane integrity and eventually the violent rupture of the cell(s).4 Necrosis generally leads to uncontrolled release of cellular components that can initiate an inflammatory response when it develops in vivo.

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