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Human APOA1 Protein expressed in Escherichia coli (E. coli) - ABIN413012
Barlic, Zhu, Murphy: Atherogenic lipids induce high-density lipoprotein uptake and cholesterol efflux in human macrophages by up-regulating transmembrane chemokine CXCL16 without engaging CXCL16-dependent cell adhesion. in Journal of immunology (Baltimore, Md. : 1950) 2009
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Human APOA1 Protein expressed in Escherichia coli (E. coli) - ABIN2003220
Soutar, Hawkins, Vigushin, Tennent, Booth, Hutton, Nguyen, Totty, Feest, Hsuan: Apolipoprotein AI mutation Arg-60 causes autosomal dominant amyloidosis. in Proceedings of the National Academy of Sciences of the United States of America 1992
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APOA1 may use a reciprocating thumbwheel-like mechanism to activate HDL-remodeling proteins
C-terminal truncation of apoA-I by chymase released from cardiac mast cells during ischemia impairs the ability of apoA-I to heal damaged endothelium in the ischemic myocardium
These results suggest that AIBP inhibits inflammatory signaling pathways through binding to apoA-1 and stabilizing ABCA1, and subsequent alteration of lipid rafts and TLR4 in the cell membrane.
Eighty-three percent of patients with a damaging mutation in ABCA1 or APOA1 had evidence of atherosclerosis compared with 38.6% with low HDL-C without such a mutation and was observed to be homozygote for an in-frame deletion of 1 amino acid in theAPOA1gene.
data suggest that Arg123 of apoA-I on discoidal HDL participates in lecithin:cholesterol acyltransferase (LCAT)-mediated cholesterol esterification
The Glu34Lys mutation promotes a shift from the "closed" to the "open" orientation of the Trp72 side chain and thus modulates structural protection of amyloid hot spots. This mutation decreases protein stability and promotes amyloidosis.
results show that adenylyl cyclase 1 is a major isoform for apoA-1-activated cAMP signaling to promote cholesterol transport and exocytosis to the surface of THP-1 macrophage foam cells
The study examined how point mutations associated with hereditary amyloidosis (F71Y and L170P) or atherosclerosis (L159R) influence the local apoA-I conformation in model lipoproteins. Mutation-induced structural perturbations in lipid-bound protein were attenuated compared to the free protein and indicated close coupling between the two belt-forming apoA-I molecules.
As the main effect of iron deregulation is proposed to be an increase in oxidative stress, we analysed the effects of iron on [1-93]ApoA-I aggregation. By using different biochemical approaches, we demonstrated that Fe(II) is able to reduce the formation of [1-93]ApoA-I fibrillar species, probably by stabilizing its monomeric form, whereas Fe(III) shows a positive effect on polypeptide fibrillogenesis.
Apo-A1-G75A-polymorphism is not necessary for the genesis, but it is a risk factor for severity of shoulder adhesive capsulitis
Oxidation of methionine residues in human apolipoprotein A-I generates a potent pro-inflammatory molecule
AIP and apo B/apo A-I associated with cIMT in NAFLD patients
Meta-analysis showed that pretreatment low ApoA-I level was related to worse survival in patients with various tumors. Serum ApoA-I level might be a powerful and noninvasive biomarker to predict cancer prognosis.
Significant prognostic risk factors for the mentioned comorbid pathologies were lipid metabolism parameters HDL-Ch, LDL-Ch, VLDL-Ch and carrier state of the +83T allele of the ApoA1 gene and Del allele of the ApoB gene.
Apolipoprotein A-I directly interacts with extracellular domain 1 of human ABCA1
HDAC3 inhibitor treatment can suppress HCV replication, an effect that was likely mediated via downregulation of Apo-A1 and upregulation of LEAP-1.
These results argue for a protective effect of EGCG on apoA-I amyloid associated with atherosclerosis and suggest that EGCG-induced remodeling of amyloid may be tightly regulated by GAGs and other amyloid co-factors in vivo, depending on EGCG bioavailability.
In conclusion, low serum APOA1 levels are associated with advanced stage and systemic inflammation, while serum APOB does not significantly correlate with tumor stage.
ApoA-I, apoB and the apoB/apoA-I ratio showed strong association with ultrasound indicators of carotid atherosclerosis in ischemic stroke patients.
Structural stability and local dynamics in disease-causing mutants of human apolipoprotein a-I: what makes the protein amyloidogenic.
Altered intestinal lymphatic HDL-ApoA-I and miR-223 metabolism in IR and modulation by niacin may provide insight into the intestinal-mediated regulation of the reverse cholesterol transport pathway
We developed a chimaeric molecule termed Fibapo in which FGF19 is covalently coupled to apolipoprotein A-I. Fibapo retains FGF19 biological activities but has significantly increased half-life and hepatotropism. Here we evaluated the pro-regenerative activity of Fibapo in two clinically relevant models where liver regeneration may be impaired: acetaminophen (APAP) poisoning, and PH in aged mice.
this study indicates that ionic interactions in the C-terminal domain of apoA-I favor self-association and that monomeric apoA-I is more active in solubilizing phospholipid bilayers.
These results suggested that apoA-I overexpression could reduce steatosis by decreasing lipid levels and by suppressing endoplasmic reticulum stress and lipogenesis in hepatocytes. ApoA-I expression could significantly reduce hepatic ER stress and lipogenesis in hepatocytes.
ABCA1-derived nascent high-density lipoprotein-apolipoprotein AI and lipids metabolically segregate.
apoA-I/ABCA1-mediated cholesterol efflux without STAT3 activation can reduce proinflammatory cytokine expression in macrophages.
a novel protective role for ApoA-I in colitis and CAC
Our results assign a novel role for 4F(apoA-I mimetic peptide ) as a modulator of the TICE pathway and suggest that the anti-inflammatory functions of 4F may be a partial consequence of the codependent intestinal transport of both 4F and cholesterol.
Preincubation of endothelial cells with apoA-I protected against the TNF-alpha-induced inhibition of HTR-8/SVneo (trophoblast) cell integration into endothelial (UtMVEC) networks. These data suggest that a healthy lipid profile may affect pregnancy outcomes by priming endothelial cells in preparation for trophoblast invasion.
Reductions in Dio1 expression reduce the expression of ApoA-I in a 3,5,3'-triiodothyronine-/thyroid hormone response element-independent manner.
apoA-1 deficiency generates changes in the bone cell precursor population that increase adipoblast, and decrease osteoblast production resulting in reduced bone mass and impaired bone quality
This study suggests that enhancement of macrophage cholesterol metabolism by PPARgammais not contributed by activating ABCA1 expression and ABCA1-mediated cholesterol efflux to apoAI, which is not involved by CD36 expression either.
Mass spectrometry analysis of peptides derived from chemically crosslinked HDL-SAA particles detected multiple crosslinks between apoA1 and SAA, indicating close proximity (within 25 A) of these two proteins on the HDL surface, providing a molecular and structural mechanism for the simultaneous binding of heparin to apoA1 and SAA.
results demonstrate that double deletion of Apoe and Apoa1 ameliorated the amyloid pathology.
study suggests that apolipoprotein a1 can alleviate obesity related metabolic disease by inducing AMPK dependent mitochondrial biogenesis.
ApoA-I can attenuate lymphocyte activation and autoimmunity in Lupus independently of cholesterol transport, through oxidized fatty acid peroxisome proliferator-activated receptor gamma ligands, and it can reduce renal inflammation in glomerulonephritis.
KLF14 regulates plasma HDL-C levels and cholesterol efflux capacity by modulating hepatic ApoA-I production.
Akt, through its downstream targets, mTORC1 and hence autophagy, negatively regulates cholesterol efflux to apoA-I.
macrophage apoAI expression protects against atherosclerosis and dermatitis by reducing cholesterol accumulation and regulating CD4(+) T-cell levels, without affecting serum HDL or tissue macrophage levels.
insulin secretion and tissue rejuvenation activities of WT-reconstituted high-density lipoproteins were nearly depleted by fructosylation, but V156K-rHDL did not lose its beneficial activity.
The NABB system using engineered zebrafish apo A-I is a native-like membrane mimetic system for G-protein-coupled receptors.
the model of a two-step process for the transendothelial transport of apoA-I in which apoA-I is initially lipidated by ABCA1 and then further processed by ABCA1-independent mechanisms.
Local HDAdApoAI vascular gene therapy may promote rapid regression of small-to-moderate-sized atherosclerotic lesions.
These differentially expressed proteins associated with key mechanisms involved in atherosclerosis and signaling mechanisms related with vitamin E.
This study showed that apoA-I exerted protective effects against fatty liver disease in rabbits induced by a high-fat diet, possibly through its antioxidant actions.
The molar ratio ApoE/ApoA-I is negatively correlated with the enzyme activity, and positively correlated with increases in the intima-media thickness of common carotid wall and cardiac dysfunction signs.
Alterations in the Apo A-I pattern is a good indicator of the presence and severity of infectious diseases in the pig.Lower overall amounts of Apo A-I were observed in Salmonella typhimurium and Escherichia coli infections.
blood level decreases during experimentally induced acute-phase processes in pigs
down-regulation of apolipoprotein A-I and A-IV messages in the liver may be mediated by interleukin 6 and tumor necrosis factor-alpha
This gene encodes apolipoprotein A-I, which is the major protein component of high density lipoprotein (HDL) in plasma. The protein promotes cholesterol efflux from tissues to the liver for excretion, and it is a cofactor for lecithin cholesterolacyltransferase (LCAT) which is responsible for the formation of most plasma cholesteryl esters. This gene is closely linked with two other apolipoprotein genes on chromosome 11. Defects in this gene are associated with HDL deficiencies, including Tangier disease, and with systemic non-neuropathic amyloidosis.
, apolipoprotein A1
, apolipoprotein A-1
, preproapolipoprotein A-I
, apolipoprotein A-I
, apolipoprotein A-I preproprotein
, Apolipoprotein A1
, apolipoprotein A-I-like
, Apolipoprotein A-I