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NGAL Antibody

Purified Mouse Monoclonal Antibody (Mab)

     
  • 1 - NGAL Antibody AP52863
    Indirect ELISA assay for anti-NGAL mouse mAb.Antigen coating concentration: 4ug/ml.
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB
Primary Accession P80188
Reactivity Human
Host Mouse
Clonality Monoclonal
Isotype IgG2b
Calculated MW 23 KDa
Additional Information
Gene ID 3934
Other Names 24p3; 25 kDa alpha-2-microglobulin-related subunit of MMP-9; HNL; Lcn2; Lipocalin 2; Lipocalin-2; Migration stimulating factor inhibitor; MSFI; Neutrophil gelatinase-associated lipocalin; NGAL; NGAL_HUMAN; Oncogene 24p3; p25; Siderocalin.
Format Purified mouse monoclonal antibody in PBS(pH 7.4) containing with 0.03% Proclin300 and 50% glycerol.
Storage Store at -20 °C.Stable for 12 months from date of receipt
Protein Information
Name LCN2
Synonyms HNL, NGAL
Function 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.
Cellular Location Secreted. Note=Upon binding to the SLC22A17 (24p3R) receptor, it is internalized
Tissue Location Expressed in bone marrow and in tissues that are prone to exposure to microorganism. High expression is found in bone marrow as well as in uterus, prostate, salivary gland, stomach, appendix, colon, trachea and lung. Not found in the small intestine or peripheral blood leukocytes
Research Areas

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.

REFERENCES

Bundgaard J.R.,et al.Biochem. Biophys. Res. Commun. 202:1468-1475(1994).
Cowland J.B.,et al.Genomics 45:17-23(1997).
Ota T.,et al.Nat. Genet. 36:40-45(2004).
Ebert L.,et al.Submitted (JUN-2004) to the EMBL/GenBank/DDBJ databases.
Humphray S.J.,et al.Nature 429:369-374(2004).

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