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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

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APOB — PRG4

Text-mined interactions from Literome

Chang et al., J Biol Chem 2000 (Arteriosclerosis) : However, it is not known whether Ox-LDL can regulate proteoglycan expression and thus affect arterial wall lipoprotein retention
Chang et al., Arterioscler Thromb Vasc Biol 2003 : We have shown that copper oxidized LDL ( Ox-LDL ) regulates proteoglycan synthesis by arterial smooth muscle cells
Akagi et al., J Orthop Res 2006 (Osteoarthritis) : In this study, we demonstrated synergistic effects of cyclic tensile stretch load and ox-LDL on cell viability and proteoglycan synthesis in chondrocytes, which may be mediated through enhanced expression of LOX-1 and which has important implications in the progression of cartilage degeneration in osteoarthritis
Gustafsson et al., Circ Res 2007 (Atherosclerosis) : Thus, retention of LDL in the artery wall is initiated by direct LDL-proteoglycan binding but shifts to indirect binding with bridging molecules such as LPL
Hiukka et al., Diabetes 2009 (Diabetes Mellitus, Type 2...) : We showed that enriching LDL with apoCIII only induced a small increase in LDL-proteoglycan binding, and this effect was dependent on a functional site A in apoB100
Sun et al., PloS one 2011 : One pathway, studied in human breast cancer cell lines, involves upregulation of the proteoglycan , syndecan-1 (SDC-1) by n-3 PUFA enriched LDL
Vijayagopal et al., Biochim Biophys Acta 1988 : Acta 837-251 ) have shown that complexes of plasma low-density lipoproteins (LDL) and arterial chondroitin sulfate-dermatan sulfate proteoglycan aggregate promote LDL degradation and cholesteryl ester accumulation in mouse peritoneal macrophages
Vijayagopal et al., Biochim Biophys Acta 1985 : The proteoglycan stimulated degradation of LDL produced a marked increase in cholesteryl ester synthesis and content in macrophages
Mas-Oliva et al., J Biol Chem 1994 : Treatment of purified PDMBP with protease or chondroitinase AC or ABC abolished the ability of the proteoglycan to inhibit the binding of AcAc LDL to macrophages
Vijayagopal et al., Biochem J 1993 (Arteriosclerosis) : Likewise, excess LDL-proteoglycan complex inhibited the binding of 125I-acetyl-LDL by 64 %