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CERID Bibliography
Fas (CD95) induces macrophage proinflammatory chemokine production via a MyD88-dependent, caspase-independent pathway. J Leukoc Biol. 2007 ;82(3):721-8.
. CARD games between virus and host get a new player. Trends Immunol. 2006 ;27(1):1-4.
. Physiological functions of caspases beyond cell death. Am J Pathol. 2006 ;169(3):729-37.
. Chlamydia pneumoniae augments the oxidized low-density lipoprotein-induced death of mouse macrophages by a caspase-independent pathway. Infect Immun. 2005 ;73(7):4315-22.
. Fas-mediated acute lung injury requires fas expression on nonmyeloid cells of the lung. J Immunol. 2005 ;175(6):4069-75.
. Role of caspases in death and survival of the plaque macrophage. Arterioscler Thromb Vasc Biol. 2005 ;25(5):895-903.
. Fas and Fas-associated death domain protein regulate monocyte chemoattractant protein-1 expression by human smooth muscle cells through caspase- and calpain-dependent release of interleukin-1alpha. Circ Res. 2003 ;93(6):515-22.
. Fas (CD95) induces proinflammatory cytokine responses by human monocytes and monocyte-derived macrophages. J Immunol. 2003 ;170(12):6209-16.
. The p17 cleaved form of caspase-3 is present within viable macrophages in vitro and in atherosclerotic plaque. Arterioscler Thromb Vasc Biol. 2003 ;23(7):1276-82.
. Cellular FLIP is expressed in cardiomyocytes and down-regulated in TUNEL-positive grafted cardiac tissues. Cardiovasc Res. 2000 ;48(1):101-10.
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