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Key Documents

SRP4693

Sigma-Aldrich

Apolipoprotein A−I human

recombinant, expressed in E. coli, ≥97% (SDS-PAGE), ≥97% (HPLC)

Sinónimos:

APOA1, Apo-AI, Apolipoprotein A-I, C117399, MGC117399

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About This Item

Número de CAS:
UNSPSC Code:
12352202
NACRES:
NA.32

biological source

human

recombinant

expressed in E. coli

assay

≥97% (HPLC)
≥97% (SDS-PAGE)

form

lyophilized

mol wt

~28 kDa

packaging

pkg of 100 μg

storage condition

avoid repeated freeze/thaw cycles

impurities

endotoxin, tested

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

Gene Information

human ... ApoA1(335)

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General description

ApoA-I (apolipoprotein A-I) is a 29.0kDa protein produced in the liver and intestine, and secreted as the predominant constituent of nascent high-density lipoprotein (HDL) particle. Recombinant human ApoA-I is a 28.2kDa protein of 244 amino acid residues.
ApoA-I, which is found exclusively in HDL, has a unique ability to capture and solubilize free cholesterol. This apoA-I ability enables HDL to remove excess peripheral cholesterol and return it to the liver for recycling and excretion. This process, called reverse cholesterol transport, is though to inhibit atherogenesis. For this reason HDL is also known as the "good cholesterol." The therapeutic potential of apoA-I has been recently assessed in patients with acute coronary syndromes, using a recombinant form of a naturally occurring variant of apoA-I (called apoA-I Milano). The availability of recombinant normal apoA-I should facilitate further investigation into the potential usefulness of apoA-I in preventing atherosclerotic vascular diseases.

Application

Apolipoprotein A-I human has been used in the cholesterol efflux assay.

Biochem/physiol Actions

ApoA-I (apolipoprotein A-I), which is found exclusively in HDL (high-density lipoprotein), has a unique ability to capture and solubilize free cholesterol. This apoA-I ability enables HDL to remove excess peripheral cholesterol and return it to the liver for recycling and excretion. This process, called reverse cholesterol transport, is thought to inhibit atherogenesis. For this reason HDL is also known as the "good cholesterol." The therapeutic potential of apoA-I has been recently assessed in patients with acute coronary syndromes, using a recombinant form of a naturally occurring variant of apoA-I (called apoA-I Milano). The availability of recombinant normal apoA-I should facilitate further investigation into the potential usefulness of apoA-I in preventing atherosclerotic vascular diseases. Changes in the level of serum apoA-I may serve as a prognostic marker for non-metastatic nasopharyngeal carcinoma. Low levels of apoA-I in the plasma is linked to hyperhomocysteinemia.

Physical form

Sterile filtered and Lyophilized without additives.

Preparation Note

Centrifuge the vial prior to opening. Avoid freeze-thaw cycles.

Reconstitution

Reconstitute in water to a concentration of 0.1-1.0 mg/ml. The solution can then be diluted into other aqueous buffers and store at 4 °C for 1 week or –20 °C for future use.

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

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Huairui Shi et al.
Scientific reports, 6, 20154-20154 (2016-01-30)
Lanatoside C's impact on atherosclerosis is poorly understood. The present study was conducted to determine whether lanatoside C affects the development of atherosclerosis in apolipoprotein E-deficient (ApoE(-/-)) mice. ApoE(-/-) mice were administered either phosphate-buffered saline (PBS) containing 0.1% DMSO (the
Targeted inactivation of hepatic Abca1 causes profound hypoalphalipoproteinemia and kidney hypercatabolism of apoA-I.
Timmins JM
The Journal of Clinical Investigation, 115, 1333-1342 (2005)
Somatic gene transfer of human ApoA-I inhibits atherosclerosis progression in mouse models.
Benoit P, et al.
Circulation, 99, 105-110 (1999)
Effect of recombinant ApoA-I Milano on coronary atherosclerosis in patients with acute coronary syndromes: a randomized controlled trial.
Nissen SE, et al.
JAMA : The Journal of the American Medical Association, 290, 2292-2300 (2003)
Centripetal cholesterol flux to the liver is dictated by events in the peripheral organs and not by the plasma high density lipoprotein or apolipoprotein A-I concentration.
Jolley CD, et al.
Journal of Lipid Research, 39, 2143-2149 (1998)

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