Biotinylated Human Angiopoietin-like 3 / ANGPTL3 Protein, His,Avitag™

Proteins and Peptides

貨號 Cat. No.
AN3-H82E7
規格 Size
200ug
品牌 Brand
ACROBiosystems
Species
Human
Conjugate
Precision Avi
Expression System
HEK293
Tag
Avi Tag 、 His Tag

Description




Source : 


Biotinylated Human Angiopoietin-like 3, His,Avitag (AN3-H82E7) is expressed from human 293 cells (HEK293). It contains AA Ser 17 - Pro 220 (Accession # Q9Y5C1-1).


 

Molecule : Angiopoietin-like 3


 

Synonyms : ANGPTL3,ANGPT5,ANG-5,Angiopoietin-5,FHBL2


 

Format : Powder


 

Category : MABSol® Biotin Labeled Proteins


 

Accession : NP_055310


 

Storage : -20℃


 

Shipping condition : Powder,RT


 

Molecular Weight : 27.4 kDa


 

Characteristics :


This protein carries a polyhistidine tag at the C-terminus, followed by an Avi tag. The protein has a calculated MW of 27.4 kDa. The protein migrates as 30-40 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.


 

Endotoxin Level : Less than 1.0 EU per μg by the LAL method.


 

Buffer : PBS, pH7.4


 

Description :


Angiopoietin-like protein 3 (ANGPTL3) is also known as Angiopoietin-related protein 3, Angiopoietin-5 (ANGPT5 / ANG-5), is a member of the angiopoietin-like family of secreted factors. ANGPTL3 / ANGPT5 is predominantly expressed in the liver, and has the characteristic structure of angiopoietins, consisting of a signal peptide, N-terminal coiled-coil domain and the C-terminal fibrinogen (FBN)-like domain. The FBN-like domain in angiopoietin-like 3 protein was shown to bind alpha-5/beta-3 integrins, and this binding induced endothelial cell adhesion and migration. This protein may also play a role in the regulation of angiogenesis. Angptl3 also acts as dual inhibitor of lipoprotein lipase (LPL) and endothelial lipase (EL), and increases plasma triglyceride and HDL cholesterol in rodents. ANGPTL3 inhibit endothelial lipase to catalyze HDL-phospholipid and increase HDL-PL levels. Circulating PL-riched HDL particles have high cholesterol efflux abilities.


 

References :


(1) Conklin D., et al., 1999, Genomics 62:477-482.
(2) Musunuru K., et al., 2010, New England Journal of Medicine 363 (23): 2220–2227.





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