Lipocalin 2 Protein (LCN2) (full length)

Produktnummer ABIN1045129

Native Lipocalin 2-Protein exprimiert in Human.

Kurzübersicht für Lipocalin 2 Protein (LCN2) (full length) (ABIN1045129)

Target: Lipocalin 2 (LCN2)

Protein-Typ: Native

Spezies: Human

Quelle: Human

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

Reinheit: > 95 %(SDS-PAGE)

Produktdetails

Proteineigenschaft: full length

Aufreinigung: Purified from human urine

Anwendungsinformationen

Applikationshinweise: calibrator ,immunogen and other possible

Kommentare:

Full length native Neutrophil gelatinase-associated lipocalin protein

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Lyophilized

Buffer: PBS

Lagerung: -20 °C

Antigendetails

Target: Lipocalin 2 (LCN2)

Andere Bezeichnung: Neutrophil gelatinase-associated lipocalin

Hintergrund: 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