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APOE — IRF6

Text-mined interactions from Literome

Van Oosten et al., J Biol Chem 2001 (Sepsis) : We now report that intravenously administered LPS strongly increases the serum levels of apoE
Saura et al., J Neurochem 2003 : LPS induced dose dependent increases in apoJ and decreases in apoE expression and secretion with maximum effects at 1-10 ng/mL and 0.1-1 microg/mL, respectively ... These data demonstrate that glial apoE and apoJ expression are independently regulated by LPS in microglia and astroglia, respectively, and that activated microglia are the predominant source of apoE in mixed glial cultures
Kay et al., Atherosclerosis 2003 (Aneurysm, Ruptured...) : These data provide novel indirect evidence suggesting that after SAH CSF Lps undergo remodelling and apoE containing Lps are selectively reduced in brain injury CSF
Wehrwein et al., Cardiovascular diabetology 2006 (Diabetes Mellitus, Type 1) : Monocytes were isolated from controls and T1D patients and the LPS stimulated increase of IL-6, CXCL8, monocyte chemotactic protein 1 ( CCL2, MCP-1 ) and superoxide dismutase ( SOD 2 ), as well as the LPS mediated decrease of apolipoprotein E (Apo E) in primary human monocytes from controls and T1D patients was determined
Maezawa et al., Journal of neuroinflammation 2006 : Our results suggest that LPS activation of innate immune response in TR APOE glia results in opposing outcomes from microglia and astrocytes as a result of TR APOE dependent activation of p38MAPK or NF-kappaB signaling in these two cell types
Hayashi et al., J Neurosci 2007 : The anti-apoptotic effect of LPs required the association of apolipoprotein E with lipids but did not require cholesterol
Gafencu et al., J Biol Chem 2007 (Inflammation) : Finally, we showed that LPS inhibited apoE gene expression via activation of the Tpl-2/MEK/ERK pathway acting on a different apoE promoter region ... In summary, LPS represses apoE gene expression in macrophages via signaling pathways that involve the upstream kinases Tpl-2 and MEKK1, the intermediate mitogen activated protein kinases ERK and JNK, and the downstream transcription factors AP-1 and NF-kappaB that inhibit the apoE promoter activity via distinct regions
Pocivavsek et al., Biochem Biophys Res Commun 2009 (Alzheimer Disease) : Reduced JNK phosphorylation is vital to overcome the LPS induced decrease in apoE expression, suggesting that JNK inhibition may be an effective way to increase apoE protein and protract its anti-inflammatory properties
Zhu et al., Biochem J 2010 : Results showed that exogenously added apoE suppressed the LPS and poly ( I-C ) induction of IL ( interleukin)-6, IL-1beta and TNF-alpha ( tumour necrosis factor-alpha ) secretion by RAW 264.7 cells
Werb et al., J Biol Chem 1983 : The suppressive effects of LPS on apo-E synthesis in culture were selective, and secretion of many other major macrophage proteins was not affected