Tabela com principais espec.
|Species Reactivity||Key Applications||Host||Format||Antibody Type|
|Ch, H, M||ELISA, IP, WB, IH(P)||M||Purified||Monoclonal Antibody|
|Presentation||Presented as a liquid in PBS, pH 7.4 with 0.05% sodium azide.|
|Safety Information according to GHS|
|Material Size||100 µg|
|Visão geral das referências||Aplicação||Pub Med ID|
|Decreased APOE-containing HDL subfractions and cholesterol efflux capacity of serum in mice lacking Pcsk9. |
Choi, S; Aljakna, A; Srivastava, U; Peterson, BR; Deng, B; Prat, A; Korstanje, R
Lipids in health and disease 12 112 2013
Studies in animals showed that PCSK9 is involved in HDL metabolism. We investigated the molecular mechanism by which PCSK9 regulates HDL cholesterol concentration and also whether Pcsk9 inactivation might affect cholesterol efflux capacity of serum and atherosclerotic fatty streak volume.Mass spectrometry and western blot were used to analyze the level of apolipoprotein E (APOE) and A1 (APOA1). A mouse model overexpressing human LDLR was used to test the effect of high levels of liver LDLR on the concentration of HDL cholesterol and APOE-containing HDL subfractions. Pcsk9 knockout males lacking LDLR and APOE were used to test whether LDLR and APOE are necessary for PCSK9-mediated HDL cholesterol regulation. We also investigated the effects of Pcsk9 inactivation on cholesterol efflux capacity of serum using THP-1 and J774.A1 macrophage foam cells and atherosclerotic fatty streak volume in the aortic sinus of Pcsk9 knockout males fed an atherogenic diet.APOE and APOA1 were reduced in the same HDL subfractions of Pcsk9 knockout and human LDLR transgenic male mice. In Pcsk9/Ldlr double-knockout mice, HDL cholesterol concentration was lower than in Ldlr knockout mice and higher than in wild-type controls. In Pcsk9/Apoe double-knockout mice, HDL cholesterol concentration was similar to that of Apoe knockout males. In Pcsk9 knockout males, THP-1 macrophage cholesterol efflux capacity of serum was reduced and the fatty streak lesion volume was similar to wild-type controls.In mice, LDLR and APOE are important factors for PCSK9-mediated HDL regulation. Our data suggest that, although LDLR plays a major role in PCSK9-mediated regulation of HDL cholesterol concentration, it is not the only mechanism and that, regardless of mechanism, APOE is essential. Pcsk9 inactivation decreases the HDL cholesterol concentration and cholesterol efflux capacity in serum, but does not increase atherosclerotic fatty streak volume.
|Cardiomyocytes undergo apoptosis in human immunodeficiency virus cardiomyopathy through mitochondrion- and death receptor-control pathways. |
Twu, C., et al.
Proc. Nat'l. Acad. Sci. U.S.A., 99(22):14386-14391 (2002) 2002
|Technical note: Aberrant detection of cell surface Fas ligand with anti-peptide antibodies. |
Smith, D., et al.
J. Immunol., 160(9):4159-60 (1998) 1998
|Death receptors: signaling and modulation. |
Ashkenazi, A., et al.
Science, 281(5381):1305-8 (1998) 1998
|Fas ligand deficiency in HIV disease. |
Sieg, S., et al.
Proc. Nat'l. Acad. Sci. USA, 94(11):5860-5 (1997) 1997
|Expression of the functional soluble form of human Fas ligand in activated lymphocytes |
Tanaka, M.,EMBO Journal (European Molecular Biology); vol. 14, No.6, 1129-1135
EMBO Journal (European Molecular Biology); vol. 14, No.6, 1129-1135 1995
Ficha de dados
|MOUSE ANTI-ABCA1 MONOCLONAL ANTIBODY|