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NGAL Antibody
Purified Mouse Monoclonal Antibody (Mab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB |
|---|---|
| Primary Accession | P80188 |
| Reactivity | Human |
| Host | Mouse |
| Clonality | Monoclonal |
| Isotype | IgG2b |
| Calculated MW | 23 KDa |
| 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 0.09% (W/V) sodium azide and 50% glycerol. |
| Storage | Store at -20 °C.Stable for 12 months from date of receipt |
| Name | LCN2 |
|---|---|
| Synonyms | HNL, NGAL {ECO:0000303|PubMed:8060329} |
| Function | Iron-trafficking protein involved in multiple processes such as apoptosis, innate immunity and renal development (PubMed:12453413, PubMed:20581821, PubMed:27780864). Binds iron through association with 2,3-dihydroxybenzoic acid (2,3-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 (By similarity). Involved in innate immunity; limits bacterial proliferation by sequestering iron bound to microbial siderophores, such as enterobactin (PubMed:27780864). Can also bind siderophores from M.tuberculosis (PubMed:15642259, PubMed:21978368). |
| Cellular Location | Secreted. Cytoplasmic granule lumen. Cytoplasmic vesicle lumen. Note=Upon binding to the SLC22A17 (24p3R) receptor, it is internalized (By similarity). Releases the bound iron in the acidic lumen of cytoplasmic vesicles (PubMed:12453413, PubMed:20581821). {ECO:0000250|UniProtKB:P11672, ECO:0000269|PubMed:12453413, ECO:0000269|PubMed:20581821} |
| Tissue Location | Detected in neutrophils (at protein level) (PubMed:7683678, PubMed:8298140). Expressed in bone marrow and in tissues that are prone to exposure to microorganism (PubMed:9339356) High expression is found in bone marrow as well as in uterus, prostate, salivary gland, stomach, appendix, colon, trachea and lung (PubMed:9339356). Expressed in the medullary tubules of the kidney (PubMed:30418175). Not found in the small intestine or peripheral blood leukocytes (PubMed:9339356). |
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Provided below are standard protocols that you may find useful for product applications.
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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