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MicroRNA-370 controls the expression of MicroRNA-122 and Cpt1α and affects lipid metabolism[S]

Journal of lipid research, 2010-06, Vol.51 (6), p.1513-1523

2010

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Role of apoA-I, ABCA1, LCAT, and SR-BI in the biogenesis of HDL

Journal of molecular medicine (Berlin, Germany), 2006-04, Vol.84 (4), p.276-294

2006

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High-density lipoprotein attenuates Th1 and th17 autoimmune responses by modulating dendritic cell maturation and function

The Journal of immunology (1950), 2015-05, Vol.194 (10), p.4676-4687

2015

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Effect of apoA-I Mutations in the Capacity of Reconstituted HDL to Promote ABCG1-Mediated Cholesterol Efflux

PloS one, 2013-06, Vol.8 (6), p.e67993-e67993

2013

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Regulation of Human Apolipoprotein M Gene Expression by Orphan and Ligand-dependent Nuclear Receptors

The Journal of biological chemistry, 2010-10, Vol.285 (40), p.30719-30730

2010

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ApoA-IV promotes the biogenesis of apoA-IV-containing HDL particles with the participation of ABCA1 and LCAT[S]

Journal of lipid research, 2013-01, Vol.54 (1), p.107-115

2013

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Biophysical analysis of apolipoprotein E3 variants linked with development of type III hyperlipoproteinemia

PloS one, 2011-11, Vol.6 (11), p.e27037

2011

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apolipoprotein E4 fragment can promote intracellular accumulation of amyloid peptide beta 42

Journal of neurochemistry, 2010-11, Vol.115 (4), p.873-884

2010

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Inflammatory Signaling Pathways Regulating ApoE Gene Expression in Macrophages

The Journal of biological chemistry, 2007-07, Vol.282 (30), p.21776-21785

2007

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Using adenovirus-mediated gene transfer to study the effect of myeloperoxidase on plasma lipid levels, HDL structure and functionality in mice expressing human apoA-I forms

Biochemical and biophysical research communications, 2022-09, Vol.622, p.108-114

2022

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apoE3[K146N/R147W] acts as a dominant negative apoE form that prevents remnant clearance and inhibits the biogenesis of HDL[S]

Journal of lipid research, 2014-07, Vol.55 (7), p.1310-1323

2014

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Specific Mutations in ABCA1 Have Discrete Effects on ABCA1 Function and Lipid Phenotypes Both In Vivo and In Vitro

Circulation research, 2006-08, Vol.99 (4), p.389-397

2006

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ApoE isoforms and carboxyl-terminal-truncated apoE4 forms affect neuronal BACE1 levels and Aβ production independently of their cholesterol efflux capacity

Biochemical journal, 2018-05, Vol.475 (10), p.1839-1859

2018

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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

Biochemical journal, 2007-08, Vol.406 (1), p.167-174

2007

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Cross-Linking and Lipid Efflux Properties of ApoA-I Mutants Suggest Direct Association between ApoA-I Helices and ABCA1

Biochemistry (Easton), 2004-02, Vol.43 (7), p.2126-2139

2004

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HDL biogenesis, remodeling, and catabolism

Handbook of experimental pharmacology, 2015, Vol.224, p.53

2015

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Molecular etiology of a dominant form of type III hyperlipoproteinemia caused by R142C substitution in apoE4[S]

Journal of lipid research, 2011-01, Vol.52 (1), p.45-56

2011

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Alteration of negatively charged residues in the 89 to 99 domain of apoA-I affects lipid homeostasis and maturation of HDL[S]

Journal of lipid research, 2011-07, Vol.52 (7), p.1363-1372

2011

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The Effects of Mutations in Helices 4 and 6 of ApoA-I on Scavenger Receptor Class B Type I (SR-BI)-mediated Cholesterol Efflux Suggest That Formation of a Productive Complex between Reconstituted High Density Lipoprotein and SR-BI Is Required for Efficient Lipid Transport

The Journal of biological chemistry, 2002-06, Vol.277 (24), p.21576-21584

2002

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Cross-inhibition of SR-BI- and ABCA1-mediated cholesterol transport by the small molecules BLT-4 and glyburide

Journal of lipid research, 2004-07, Vol.45 (7), p.1256-1265

2004

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Identification of the Molecular Target of Small Molecule Inhibitors of HDL Receptor SR-BI Activity

Biochemistry (Easton), 2008-01, Vol.47 (1), p.460-472

2008

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Inhibition of c-Jun-N-terminal Kinase Increases Cardiac Peroxisome Proliferator-activated Receptor α Expression and Fatty Acid Oxidation and Prevents Lipopolysaccharide-induced Heart Dysfunction

The Journal of biological chemistry, 2011-10, Vol.286 (42), p.36331-36339

2011

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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 Mutation

Biochemistry (Easton), 2006-01, Vol.45 (4), p.1242-1254

2006

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The Effect of Natural LCAT Mutations on the Biogenesis of HDL

Biochemistry (Easton), 2015-06, Vol.54 (21), p.3348-3359

2015

Volltextzugriff (PDF)

A Dominant Negative Form of the Transcription Factor c-Jun Affects Genes That Have Opposing Effects on Lipid Homeostasis in Mice

The Journal of biological chemistry, 2007-07, Vol.282 (27), p.19556-19564

2007

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MicroRNA-370 controls the expression of MicroRNA-122 and Cpt1α and affects lipid metabolism[S]

Role of apoA-I, ABCA1, LCAT, and SR-BI in the biogenesis of HDL

High-density lipoprotein attenuates Th1 and th17 autoimmune responses by modulating dendritic cell maturation and function

Effect of apoA-I Mutations in the Capacity of Reconstituted HDL to Promote ABCG1-Mediated Cholesterol Efflux

Regulation of Human Apolipoprotein M Gene Expression by Orphan and Ligand-dependent Nuclear Receptors

ApoA-IV promotes the biogenesis of apoA-IV-containing HDL particles with the participation of ABCA1 and LCAT[S]

Biophysical analysis of apolipoprotein E3 variants linked with development of type III hyperlipoproteinemia

apolipoprotein E4 fragment can promote intracellular accumulation of amyloid peptide beta 42

Inflammatory Signaling Pathways Regulating ApoE Gene Expression in Macrophages

Using adenovirus-mediated gene transfer to study the effect of myeloperoxidase on plasma lipid levels, HDL structure and functionality in mice expressing human apoA-I forms

apoE3[K146N/R147W] acts as a dominant negative apoE form that prevents remnant clearance and inhibits the biogenesis of HDL[S]

Specific Mutations in ABCA1 Have Discrete Effects on ABCA1 Function and Lipid Phenotypes Both In Vivo and In Vitro

ApoE isoforms and carboxyl-terminal-truncated apoE4 forms affect neuronal BACE1 levels and Aβ production independently of their cholesterol efflux capacity

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

Cross-Linking and Lipid Efflux Properties of ApoA-I Mutants Suggest Direct Association between ApoA-I Helices and ABCA1

HDL biogenesis, remodeling, and catabolism

Molecular etiology of a dominant form of type III hyperlipoproteinemia caused by R142C substitution in apoE4[S]

Alteration of negatively charged residues in the 89 to 99 domain of apoA-I affects lipid homeostasis and maturation of HDL[S]

The Effects of Mutations in Helices 4 and 6 of ApoA-I on Scavenger Receptor Class B Type I (SR-BI)-mediated Cholesterol Efflux Suggest That Formation of a Productive Complex between Reconstituted High Density Lipoprotein and SR-BI Is Required for Efficient Lipid Transport

Cross-inhibition of SR-BI- and ABCA1-mediated cholesterol transport by the small molecules BLT-4 and glyburide

Identification of the Molecular Target of Small Molecule Inhibitors of HDL Receptor SR-BI Activity

Inhibition of c-Jun-N-terminal Kinase Increases Cardiac Peroxisome Proliferator-activated Receptor α Expression and Fatty Acid Oxidation and Prevents Lipopolysaccharide-induced Heart Dysfunction

Structure and Stability of Apolipoprotein A-I in Solution and in Discoidal High-Density Lipoprotein Probed by Double Charge Ablation and Deletion Mutation

The Effect of Natural LCAT Mutations on the Biogenesis of HDL

A Dominant Negative Form of the Transcription Factor c-Jun Affects Genes That Have Opposing Effects on Lipid Homeostasis in Mice

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