Anti-LCN2 polyclonal antibody [Biotin] (DPABY-426)

Goat Anti-Rat LCN2 polyclonal antibody for WB, ELISA(Det)


Host Species
Antibody Isotype
Species Reactivity
Mouse myeloma cell line NS0-derived recombinant rat Lipocalin-2/NGAL. Gln21-Asn198 Accession Number P30152


Application Notes
Western Blot 0.1 μg/mL; ELISA Capture 0.2-0.8 μg/mL; ELISA Detection 0.1-0.4 μg/mL
We recommend the following for sandwich ELISA (Capture - Detection):
DPABY-287 - DPABY-426
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.


Alternative Names
LCN2; lipocalin 2; Sip24; neutrophil gelatinase-associated lipocalin; p25; NGAL
Entrez Gene ID
UniProt ID


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Lipocalin 2 (Lcn2) interferes with iron uptake by Brucella abortus and dampens immunoregulation during infection of RAW 264.7 macrophages


Authors: Huynh Tan Hop; Arayan, Lauren Togonon; Tran Xuan Ngoc Huy; Reyes, Alisha Wehdnesday Bernardo; Baek, Eun Jin; Min, Wongi; Lee, Hu Jang; Rhee, Man Hee; Watanabe, Kenta; Chang, Hong Hee; Kim, Suk

Lipocalin 2 (Lcn2) is an important innate immunity component against bacterial pathogens. In this study, we report that Lcn2 is induced by Brucella (B.) abortus infection and significantly contributes to the restriction of intracellular survival of Brucella in macrophages. We found that Lcn2 prevented iron uptake by B.abortus through two distinct mechanisms. First, Lcn2 is secreted to capture bacterial siderophore(s) and abrogate iron import by Brucella. Second, Lcn2 decreases the intracellular iron levels during Brucella infection, which probably deprives the invading Brucella of the iron source needed for growth. Suppression of Lcn2 signalling resulted in a marked induction of anti-inflammatory cytokine, interleukin 10, which was shown to play a major role in Lcn2-induced antibrucella immunity. Similarly, interleukin 6 was also found to be increased when Lcn2 signalling is abrogated; however, this induction was thought to be an alternative pathway that rescues the cell from infection when the effective Lnc2 pathway is repressed. Furthermore, Lcn2 deficiency also caused a marked decrease in brucellacidal effectors, such as reactive oxygen species and nitric oxide but not the phagolysosome fusion. Taken together, our results indicate that Lcn2 is required for the efficient restriction of intracellular B.abortus growth that is through limiting iron acquisition and shifting cells to pro-inflammatory brucellacidal activity in murine macrophages.

Effects of Ectopic Expression of NGAL on Doxorubicin Sensitivity


Authors: Chappell, William H.; Abrams, Stephen L.; Montalto, Giuseppe; Cervello, Melchiorre; Martelli, Alberto M.; Candido, Saverio; Libra, Massimo; Polesel, Jerry; Talamini, Renato; Arlinghaus, Ralph; Steelman, Linda S.; McCubrey, James A.

Neutrophil gelatinase-associated lipocalin (NGAL, a.k.a Lnc2) is a member of the lipocalin family which has diverse roles including stabilizing matrix metalloproteinase-9 from auto-degradation and as siderocalins which are important in the transport of iron. NGAL also has important biological functions involved in immunity and inflammation as well as responses to kidney damage. NGAL expression has also been associated with certain neoplasia and is important in the metastasis of breast cancer. Many advanced cancer patients have elevated levels of NGAL in their urine and it has been proposed that NGAL may be a prognostic indicator for certain cancers (e.g. breast, brain, and others). NGAL expression is detected in response to various chemotherapeutic drugs including doxorubicin and docetaxel. We were interested in the roles of NGAL expression in cancer and whether it is associated with chemotherapeutic drug resistance. In the present study, we investigated whether increased NGAL expression led to resistance to the chemotherapeutic drug doxorubicin in normal breast epithelial cells (MCF-10A), breast cancer cells (MCF-7), and colorectal cancer cells (HT-29). We infected the various cell lines with a retrovirus encoding NGAL which we constructed. Increased NGAL expression was readily detected in the NGAL-infected cells but not the empty vector-infected cells. However, increased NGAL expression did not alter the sensitivity of the cells to the chemotherapeutic drug doxorubicin. Thus, although NGAL expression is often detected after chemotherapeutic drug treatment, it by itself, does not lead to doxorubicin resistance.

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