Deletions of helices 2 and 3 of human apoA-I are associated with severe dyslipidemia following adenovirus-mediated gene transfer in apoA-I-deficient mice.
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Structure and stability of apolipoprotein a-I in solution and in discoidal high-density lipoprotein probed by double charge ablation and deletion mutationMolecular etiology of a dominant form of type III hyperlipoproteinemia caused by R142C substitution in apoE4Domains of apoE4 required for the biogenesis of apoE-containing HDL.Alteration of negatively charged residues in the 89 to 99 domain of apoA-I affects lipid homeostasis and maturation of HDL.Binding of human apoA-I[K107del] variant to TG-rich particles: implications for mechanisms underlying hypertriglyceridemia.The carboxy-terminal region of apoA-I is required for the ABCA1-dependent formation of alpha-HDL but not prebeta-HDL particles in vivo.Discrete roles of apoA-I and apoE in the biogenesis of HDL species: lessons learned from gene transfer studies in different mouse models.Differential effects of 24-hydroxycholesterol and 27-hydroxycholesterol on beta-amyloid precursor protein levels and processing in human neuroblastoma SH-SY5Y cells.Role of the hydrophobic and charged residues in the 218-226 region of apoA-I in the biogenesis of HDLSignificance of the hydrophobic residues 225-230 of apoA-I for the biogenesis of HDL.Residues Leu261, Trp264, and Phe265 account for apolipoprotein E-induced dyslipidemia and affect the formation of apolipoprotein E-containing high-density lipoprotein.Biophysical properties of apolipoprotein E4 variants: implications in molecular mechanisms of correction of hypertriglyceridemia.Naturally occurring and bioengineered apoA-I mutations that inhibit the conversion of discoidal to spherical HDL: the abnormal HDL phenotypes can be corrected by treatment with LCAT.Pathway of biogenesis of apolipoprotein E-containing HDL in vivo with the participation of ABCA1 and LCAT.Sequence-specific apolipoprotein A-I effects on lecithin:cholesterol acyltransferase activity.
P2860
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P2860
Deletions of helices 2 and 3 of human apoA-I are associated with severe dyslipidemia following adenovirus-mediated gene transfer in apoA-I-deficient mice.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
2005年论文
@zh
2005年论文
@zh-cn
name
Deletions of helices 2 and 3 o ...... sfer in apoA-I-deficient mice.
@en
type
label
Deletions of helices 2 and 3 o ...... sfer in apoA-I-deficient mice.
@en
prefLabel
Deletions of helices 2 and 3 o ...... sfer in apoA-I-deficient mice.
@en
P2093
P356
P1433
P1476
Deletions of helices 2 and 3 o ...... nsfer in apoA-I-deficient mice
@en
P2093
Adelina Shkodrani
Angeliki Chroni
Horng-Yuan Kan
P304
P356
10.1021/BI047998L
P407
P577
2005-03-01T00:00:00Z