|Tested species reactivity||Human, Mouse|
|Published species reactivity||Human|
|Host / Isotype||Rabbit / IgG|
|Immunogen||KLH conjugated synthetic peptide between 138-167 amino acids from the central region of human ANGPTL4|
|Purification||Protein A, Affinity chromatography|
|Contains||0.09% sodium azide|
|Storage Conditions||-20° C, Avoid Freeze/Thaw Cycles|
|Tested Applications||Dilution *|
|Flow Cytometry (Flow)||1:25|
|Immunohistochemistry (Paraffin) (IHC (P))||1:50-1:100|
|Western Blot (WB)||1:1000|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
|Immunohistochemistry (Paraffin) (IHC (P))||See 1 publications below|
ANGPTL4 is a member of the angiopoietin/angiopoietin-like gene family and encodes a glycosylated, secreted protein with a fibrinogen C-terminal domain. This protein is induced under hypoxic conditions in endothelial cells and is the target of peroxisome proliferation activators. The encoded protein is a serum hormone directly involved in regulating glucose homeostasis, lipid metabolism, and insulin sensitivity and also acts as an apoptosis survival factor for vascular endothelial cells. The encoded protein may play a role in several cancers and it also has been shown to prevent the metastatic process by inhibiting vascular activity as well as tumor cell motility and invasiveness. Decreased expression of this protein has been associated with type 2 diabetes.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
ANGPTL4 deficiency in haematopoietic cells promotes monocyte expansion and atherosclerosis progression.
PA5-26216 was used in immunohistochemistry - paraffin section elucidate how hematopoietic ANGPTL4 deficiency increases atherogenesis
|Aryal B,Rotllan N,Araldi E,Ramírez CM,He S,Chousterman BG,Fenn AM,Wanschel A,Madrigal-Matute J,Warrier N,Martín-Ventura JL,Swirski FK,Suárez Y,Fernández-Hernando C||Nature communications (7:null)||2016|