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Oliver E. Hutt Jun Inagaki Bollu S. Reddy Sajiv K. Nair Emily A. Reiff John T. Henri Jack F. Greiner David G. VanderVelde Ting-Lan Chiu Elizabeth A. Amin Richard H. Himes Gunda I. Georg 《Bioorganic & medicinal chemistry letters》2009,19(12):3293-3296
The total synthesis of 22-(3-azidobenzoyloxy)methyl epothilone C is described as a potential photoaffinity probe to elucidate the β-tubulin binding site. A sequential Suzuki-aldol-Yamaguchi macrolactonization strategy was utilized employing a novel derivatized C1–C6 fragment. The C22-functionalized analog exhibited good activity in microtubule assembly assays, but cytotoxicity was significantly reduced. Molecular modeling simulations indicated that excessive steric bulk in the C22 position is accommodated by the large hydrophobic pocket of the binding site. Photoaffinity labeling studies were inconclusive suggesting non-specific labeling. 相似文献
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Hutt OE Reddy BS Nair SK Reiff EA Henri JT Greiner JF Chiu TL Vandervelde DG Amin EA Himes RH Georg GI 《Bioorganic & medicinal chemistry letters》2008,18(17):4904-4906
The total synthesis of C25-benzyloxy epothilone C is described. A sequential Suzuki–Aldol–Yamaguchi macrolactonization strategy was utilized employing a novel derivatized C8–C12 fragment. The C25-benzyloxy analog exhibited significantly reduced biological activity in microtubule assembly and cytotoxicity assays. Molecular modeling simulations indicated that excessive steric bulk in the C25 position may reduce activity by disrupting key hydrogen bonds that are crucial for epothilone binding to β-tubulin. 相似文献
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Rodriguez W Mold C Kataranovski M Hutt JA Marnell LL Verbeek JS Du Clos TW 《Journal of immunology (Baltimore, Md. : 1950)》2007,178(1):530-538
C-reactive protein (CRP) is a member of the pentraxin family of proteins and an acute phase reactant. CRP modulates the response to inflammatory stimuli including LPS and C5a. We recently demonstrated that CRP prevents and reverses proteinuria in accelerated nephrotoxic nephritis (NTN). NTN is a model of active inflammatory immune complex-mediated nephritis induced by injection of antiglomerular basement membrane. CRP treatment prevented the induction of NTN in C57BL/6 (B6) mice, increased survival, and reversed ongoing nephritis. Protection was associated with a decrease in IL-1beta and chemokines in the kidney and peritoneal cells as measured by quantitative RT-PCR. However, IL-10(-/-) mice were not protected by CRP either when given before disease onset or when disease activity was maximal. FcgammaRI(-/-) mice developed NTN, but were only transiently protected by CRP treatment. This transient protection was abrogated by cobra venom factor depletion of complement from FcgammaRI(-/-) mice. However, complement depletion did not prevent CRP-mediated protection in B6 mice, and CRP was protective in C3(-/-) mice. The role of macrophages in the protection provided by CRP was tested by treating B6 mice with liposomes containing clodronate. Clodronate-containing liposomes deplete mice of splenic and hepatic macrophages for 5-7 days. Pretreatment of NTN mice with clodronate but not control liposomes completely prevented CRP-mediated protection. These studies suggest that CRP mediates protection from NTN through the induction of IL-10 and that macrophages are required. In addition, FcgammaRI plays an important role but is not the sole mediator of CRP-mediated protection. 相似文献
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