2003
DOI: 10.1074/jbc.m302309200
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Tumor Necrosis Factor-α Induces Functionally Active Hyaluronan-adhesive CD44 by Activating Sialidase through p38 Mitogen-activated Protein Kinase in Lipopolysaccharide-stimulated Human Monocytic Cells

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Cited by 78 publications
(78 citation statements)
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“…In those cells, lipopolysaccharide-induced sialydase activity is dependent on p42/p44 MAPK-mediated tumor necrosis factor ␣ (TNF␣) production. Subsequently, the TNF␣ that is produced mediates p38 MAPK activation, which then induces sialydase activity (40). TNF␣ plays a key role in GPA, and its increased level is associated with disease activity (41).…”
Section: Discussionmentioning
confidence: 99%
“…In those cells, lipopolysaccharide-induced sialydase activity is dependent on p42/p44 MAPK-mediated tumor necrosis factor ␣ (TNF␣) production. Subsequently, the TNF␣ that is produced mediates p38 MAPK activation, which then induces sialydase activity (40). TNF␣ plays a key role in GPA, and its increased level is associated with disease activity (41).…”
Section: Discussionmentioning
confidence: 99%
“…Lipopolysaccharide (LPS) and some cytokines (as tumor necrosis factor, TNF) can induce formation of a hyaluronan-adhesive form of CD44 [57]. Such cell surface receptor CD44 is needed for polymorphonuclear leukocytes to interact and migrate on hyaluronan [58].…”
mentioning
confidence: 99%
“…Chronic aggressive hepatitis is a significant risk factor of HCC recurrence following hepatectomy (22). Notably, the expression of LYVE-1 in the lymphatic endothelium is downregulated by the pro-inflammatory cytokine tumor necrosis factor-α in vitro and in vivo (23)(24)(25), suggesting that LYVE-1 expression may be suppressed by hepatitis. The fact that inflammation is initiated early during the course of liver disease is consistent with our hypothesis that LYVE-1 may be an early marker of HCC tumorigenesis.…”
Section: Univariate Analysis ----------------------------------------mentioning
confidence: 98%