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Apolipoprotein A-I (APOA1) (Active) Protein

Details for Product No. ABIN413014, Supplier: Log in to see
Protein Name
Origin
Human
61
9
4
3
3
2
2
2
2
1
1
1
1
1
1
1
1
1
1
1
1
1
Source
Escherichia coli (E. coli)
34
24
20
4
3
3
2
1
1
1
Protein Type
Recombinant
Biological Activity
Active
Application
High Pressure Liquid Chromatography (HPLC), SDS-PAGE (SDS)
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Characteristics 28.2 kDa
Biological Activity: Test in process
Purity ≥97 %
Sterility Sterile filtered
Endotoxin Level <0.1 ng/μg
Background ApoA-I is a 29.0 kDa protein produced in the liver and intestine, and secreted as the predominant constituent of nascent high-density lipoprotein (HDL) particle. 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 \\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\
Molecular Weight 28.2 kDa
Gene ID 335
NCBI Accession NM_000039
Pathways
Application Notes Optimal working dilution should be determined by the investigator.
Comment

physical form description: Sterile filtered and lyophilized with no additives

Restrictions For Research Use only
Format Lyophilized
Reconstitution Reconstitute in H₂O 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.
Handling Advice Centrifuge the vial prior to opening.
Storage -20 °C
Expiry Date 12 months
Supplier Images
Western Blotting (WB) image for Apolipoprotein A-I (APOA1) (Active) Protein (ABIN413014) Apolipoprotein A-I (APOA1) (Active) protein
Product cited in: de Haan, Karasinska, Ruddle et al.: "Hepatic ABCA1 expression improves β-cell function and glucose tolerance." in: Diabetes, Vol. 63, Issue 12, pp. 4076-82, 2014 (PubMed).

Saeed, Otsuka, Polavarapu et al.: "Pharmacological suppression of hepcidin increases macrophage cholesterol efflux and reduces foam cell formation and atherosclerosis." in: Arteriosclerosis, thrombosis, and vascular biology, Vol. 32, Issue 2, pp. 299-307, 2012 (PubMed).

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), Vol. 182, Issue 12, pp. 7928-36, 2009 (PubMed).