We have a suspicion that you are an automated web bot software, not a real user. To keep our site fast for other users, we have slowed down this page. The slowdown will gradually disappear. If you think this is a mistake, please contact us at genome-www@soe.ucsc.edu. Also note that all data for hgGeneGraph can be obtained through our public MySQL server and all our software source code is available and can be installed locally onto your own computer. If you are unsure how to use these resources, do not hesitate to contact us.
UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to APOB

APOB — PRG2

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 %