|1.||Qin, Yang: 4 articles (11/2015 - 09/2009)|
|2.||Wei, Ling: 3 articles (11/2015 - 03/2011)|
|3.||Li, Ran: 2 articles (11/2015 - 05/2014)|
|4.||Weinstein, Michael M: 2 articles (11/2011 - 12/2010)|
|5.||Young, Stephen G: 2 articles (11/2011 - 12/2010)|
|6.||Mortensen, Anne Skjetne: 2 articles (03/2008 - 03/2007)|
|7.||Arukwe, Augustine: 2 articles (03/2008 - 03/2007)|
|8.||Hilgendorf, Inken: 2 articles (07/2003 - 01/2003)|
|9.||Kruse, Charli: 2 articles (07/2003 - 01/2003)|
|10.||Zhao, Rongce: 1 article (11/2015)|
|1.||Hepatocellular Carcinoma (Hepatoma)
11/01/2015 - "The expression of vigilin was previously reported to elevate in highly proliferating tissues and increased in a subset of hepatocellular carcinoma patients. "
03/01/2011 - "[Expression of vigilin in cell lines and human hepatocellular carcinoma]."
09/01/2009 - "[VIGILIN involves in regulation of imprinting gene IGF2 and H19 in human hepatocellular carcinoma cell]."
05/01/2014 - "Vigilin is overexpressed in hepatocellular carcinoma and is required for HCC cell proliferation and tumor growth."
03/01/2011 - "The samples of 59 hepatocellular carcinoma tissues, 59 adjacent liver tissues and 33 distant non-tumor liver tissues were collected, Vigilin expression in the above samples was detected by immunohistochemistry. "
03/01/2011 - "Highly expression of Vigilin was observed in 54% of tumor tissues, 35% adjacement tissues, and 6% of distant non-tumor tissues, respectively. "
03/01/2011 - "Most of the hepatic cells expressed Vigilin, but the expression levels were different (tumor tissues: 0.2226 +/- 0.054, adjacent tissues: 0.2060 +/- 0.056, distant tissues: 0.1820 +/- 0.038, P < 0.001). "
05/01/2014 - "We also found that vigilin knockdown effectively inhibited the growth of BEL7402 cell-derived xenograft tumors in nude mice by decreasing the proliferation and increasing the apoptosis of the BEL7402 HCC cells. "
05/01/2014 - "We further investigated the impact of vigilin knockdown on HCC cell proliferation, survival, motility, tumor growth and sensitivity to chemotherapy. "
05/01/2014 - "We discovered that vigilin expression increased progressively from the liver cirrhosis tissue to adjacent non-tumor liver tissue and then to HCC tumor cells. "
11/01/2011 - "Interest in lipolysis and the metabolism of triglyceride-rich lipoproteins was recently reignited by the discovery of severe hypertriglyceridemia (chylomicronemia) in glycosylphosphatidylinositol-anchored high density lipoprotein-binding protein 1 (GPIHBP1)-deficient mice. "
12/01/2010 - "Intravenous injection of apolipoprotein A-V reconstituted high-density lipoprotein decreases hypertriglyceridemia in apoav-/- mice and requires glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1."
01/01/2015 - "To elucidate the underlying mechanism of gestational hypertriglyceridemic pancreatitis, we undertook DNA mutation analysis of the lipoprotein lipase (LPL), apolipoprotein C2 (APOC2), apolipoprotein A5 (APOA5), lipase maturation factor 1 (LMF1), and glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 (GPIHBP1) genes in five unrelated pregnant Chinese women with severe hypertriglyceridemia and pancreatitis. "
03/01/2008 - "Our data showed increased levels of ER-mediated gene expression (vitellogenin: Vtg, zona radiata protein: Zr-protein, ERalpha, ERbeta and vigilin) as well as increased cellular ERalpha protein levels after treatment with NP and PCB126, singly or in combination. "
03/01/2007 - "Quantitative real-time polymerase chain reactions confirmed the changes in expression of ERalpha, ERbeta, vitellogenin (Vtg), zona radiata protein (Zr-protein), and vigilin for the ER pathway and AhRalpha, AhRbeta, AhRR, ARNT, CYP1A1, UDPGT, and a 20S proteasome beta-subunit for the AhR pathway. "
|5.||Type 2 Diabetes Mellitus (MODY)
05/01/2012 - "Effects of hyperinsulinemia on lipoprotein lipase, angiopoietin-like protein 4, and glycosylphosphatidylinositol-anchored high-density lipoprotein binding protein 1 in subjects with and without type 2 diabetes mellitus."
06/01/2015 - "The first form is very rare monogenic early-onset chylomicronaemia, which presents in childhood or adolescence and is often caused by homozygous mutations in the gene encoding lipoprotein lipase (LPL), its cofactors apolipoprotein C-II or apolipoprotein A-V, the LPL chaperone lipase maturation factor 1 or glycosylphosphatidylinositol-anchored high density lipoprotein-binding protein 1. The second form, polygenic late-onset chylomicronaemia, which is caused by an accumulation of several genetic variants, can be exacerbated by secondary factors, such as poor diet, obesity, alcohol intake and uncontrolled type 1 or type 2 diabetes mellitus, and is more common than early-onset chylomicronaemia. "
|2.||Lipoprotein Lipase (Diacylglycerol Lipase)
|3.||Apolipoprotein C-II (ApoC2)
|4.||Messenger RNA (mRNA)
|6.||Lipase (Acid Lipase)
|8.||Apoprotein(a) (Apolipoprotein (a))
|9.||Estrogen Receptor beta
|10.||Estrogen Receptor alpha
|1.||Heterologous Transplantation (Xenotransplantation)
|3.||Drug Therapy (Chemotherapy)