TUMOR NECROSIS FACTOR

skin via distinct mechanisms. Mol Cell Biol 24, 5733–5745.26 Fomenkov A, Zangen R, Huang YP, Osada M, Guo Z,Fomenkov T, Trink B, Sidransky D & Ratovitski EA(2004) RACK1 and stratifin target DeltaNp63alpha fora proteasome degradation in head and neck squamouscell carcinoma cells upon DNA damag[r]

p65 and p50 confirmed Rnf33 down-regulation by p65 ⁄ p50. Spermatogenesisis regulated by a wide range of stimuli, including NF-jB, which, in turn, isregulated by other signals. Hence, demonstration of NF-jB-regulated Rnf33expression in testicular cells, particularly in Sertoli cells, implicates funct[r]

29. Kitazawa M, Oddo S, Yamasaki TR, Green KN, LaFerla FM: Lipopol-ysaccharide-induced inflammation exacerbates tau pathol-ogy by a cyclin-dependent kinase 5-mediated pathway in atransgenic model of Alzheimer's disease. J Neurosci 2005,25:8843-8853.30. Zhao B, Schwartz JP: Involvement of cytokines i[r]

sequence 1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; IFN, interferon; IRF-1, interferon regulatory factor-1; NF-jB, nuclearfactor-jB; shRNA, short hairpin RNA; TNF-a, tumor necrosis factor-a; TNF-R1, tumor necrosis factor receptor-1.4396 FEBS[r]

Catalytic digestion of human tumor necrosis factor-a byantibody heavy chainEmi Hifumi1,2, Kyohei Higashi3and Taizo Uda2,31 Research Center for Applied Medical Engineering, Oita University, Japan2 CREST of JST (Japan Science and Technology Corporation), Kawaguchi, Saitama, Japan3[r]

Biol Med 2002, 32:1264-75.36. Perry G, Nunomura A, Hirai K, Takeda A, Aliev G, Smith MA: Oxi-dative damage in Alzheimer's disease: the metabolicdimension. Int J Dev Neurosci 2000, 18:417-21.37. Gold BG, Udina E, Bourdette D, Navarro X: Neuroregenerativeand neuroprotective actions of neuroimmunophili[r]

deficiency leads to tracheal malformation with resulting alterationsin air flow to the lungs. Am. J. Pathol. 157, 679–688.14. Regnier, C.H., Tomasetto, C., Moog-Lutz, C., Chenard, M.P.,Wendling, C., Basset, P. & Rio, M.C. (1995) Presence of a newconserved domain in CART1, a novel member of the[r]

19. Ramilo O, Saez-Llorens X, Mertsola J, Jafari H, Olsen KD, Hansen EJ,Yoshinaga M, Ohkawara S, Nariuchi H, McCracken Jr, G.H.: Tumornecrosis factor alpha / cachectin and interleukin 1 beta initi-ate meningeal inflammation. J Exp Med 1990, 172:497-507.20. Saukkonen K, Sande S, Cioffe C, Wolp[r]

23. Yoshimura, T. & Sone, S. (1987) Different and synergistic actionsof human tumor necrosis factor and interferon-c in damage ofliposome membranes. J. Biol. Chem. 262, 4597–4601.24. Baldwin, R.L., Stolowitz, M.L., Hood, L. & Wisnieski, B.J. (1996)Structural chang[r]

JNK, c-Jun N-terminal kinase; NF-jB, nuclear factor kappa B; NIK, NF-jB-inducing kinase; RIP, receptor interacting protein; TNF, tumornecrosis factor; TNFR1 ⁄ 2, tumor necrosis factor receptor 1 ⁄ 2; TRADD, TNF receptor-associated death domain; TRAF1 ⁄ 2 ⁄ 3,TNF re[r]

Embelin, a quinone derivative, is found in the fruits of Embelia ribes Burm (Myrsinaceae). It has been shown to have a variety of therapeutic potentials including anthelmintic, anti-tumor, anti-diabetic, anti-bacterial and anti-inflammation. Inflammation is an immunological response to external harm[r]

R (TIR) domains, which also bind to TIRAP (TIR domain-containing adaptor protein), a molecule that participates in the transduction of signals from TLR4. The MyD88/TIRAP complex activates signal-transducing molecules such as IRAK1 and IRAK4 (IL-1Rc-associated kinases 1 and 4); TRAF-6 (tumor <[r]

gel-to-liquid crystalline phase transition behavior of thehydrocarbon chains with Tc¼ 30 °C for MfGl-II as well asfor LPS exhibits high similarity between the two glycolipids.A lipopolysaccharide-binding protein (LBP)-mediatedincorporation into negatively charged liposomes is observedfor both glycol[r]

Chronic inflammation and repeated infection with Opisthorchis viverrini (O. viverrini) induces intrahepatic cholangiocarcinoma (ICC). Inflammatory cytokines such as interleukin (IL) and tumor necrosis factor (TNF) are substances in the immune system that promote inflammation and causes disease to pr[r]

dạng tự do không liên kết càng cao thì càng dễ bị kết tủa ở nhiệt độ thấp, sự có mặt của chondroetin trong dịch khớp và sụn làm tăng kết tủa của axit uric. Các tinh thể kết tủa trong khớp tạo thành các dị vật vi tinh thể nhỏ kích thích đại thực bào. Các tế bào này bị tổn thương giải phóng các mediat[r]

scription and surface expression of DR5. Transient knockdown of thetranscription factor GADD153⁄ C ⁄ EBP homologous protein and applica-tion of the synthetic c-Jun N-terminal kinase inhibitor SP600125 indicatedthat enhanced DR5 expression occurred independently of GADD153 ⁄C ⁄ EBP homologous[r]

Chapter 114. Molecular Mechanisms of Microbial Pathogenesis (Part 3) Viral Adhesins (See also Chap. 161) All viral pathogens must bind to host cells, enter them, and replicate within them. Viral coat proteins serve as the ligands for cellular entry, and more than one ligand-receptor interaction may[r]

plicated and warrants extensive studies. In general, activation of NF-κB in neuronsprotects them against degeneration, but activation of NF-κB in microglia promotesneuronal degeneration. Hence, ideal agents to target NF-κB should be cell type-selective in their actions. For example, inhibitors of NF[r]