Lipocalin 2 Protein (LCN2) (full length)

Catalog No. ABIN1045129

Native Lipocalin 2 protein expressed in Human.

Quick Overview for Lipocalin 2 Protein (LCN2) (full length) (ABIN1045129)

Target: Lipocalin 2 (LCN2)

Protein Type: Native

Origin: Human

Source: Human

Application: Western Blotting (WB), SDS-PAGE (SDS), ELISA, Latex enhanced turbidimetric Immunoassay (LETIA)

Purity: > 95 %(SDS-PAGE)

Product Details

Protein Characteristics: full length

Purification: Purified from human urine

Application Details

Application Notes: calibrator ,immunogen and other possible

Comment:

Full length native Neutrophil gelatinase-associated lipocalin protein

Restrictions: For Research Use only

Handling

Format: Lyophilized

Buffer: PBS

Storage: -20 °C

Target Details

Target: Lipocalin 2 (LCN2)

Alternative Name: Neutrophil gelatinase-associated lipocalin

Background: Iron-trafficking protein involved in multiple processes such as apoptosis, innate immunity and renal development. Binds iron through association with 2,5-dihydroxybenzoic acid (2,5-DHBA), a siderophore that shares structural similarities with bacterial enterobactin, and delivers or removes iron from the cell, depending on the context. Iron-bound form (holo-24p3) is internalized following binding to the SLC22A17 (24p3R) receptor, leading to release of iron and subsequent increase of intracellular iron concentration. In contrast, association of the iron-free form (apo-24p3) with the SLC22A17 (24p3R) receptor is followed by association with an intracellular siderophore, iron chelation and iron transfer to the extracellular medium, thereby reducing intracellular iron concentration. Involved in apoptosis due to interleukin-3 (IL3) deprivation: iron-loaded form increases intracellular iron concentration without promoting apoptosis, while iron-free form decreases intracellular iron levels, inducing expression of the proapoptotic protein BCL2L11/BIM, resulting in apoptosis. Involved in innate immunity, possibly by sequestrating iron, leading to limit bacterial growth.

Pathways: Cellular Response to Molecule of Bacterial Origin, Transition Metal Ion Homeostasis