LCN2 Antibodies

Neutrophil gelatinase-associated lipocalin (LCN2)

Iron-trafficking protein involved in multiple processes such as apoptosis, innate immunity and renal growth. 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) together 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.

Gene Information

Human
Gene Name:	LCN2
Uniprot:	P80188
Entrez:	3934

Family

Belongs to:
calycin superfamily

Alternative Names

24p3; 25 kDa alpha-2-microglobulin-related subunit of MMP-9; HNL; LCN2; lipocalin 2 (oncogene 24p3); lipocalin 2; Lipocalin2; Lipocalin-2; migration-stimulating factor inhibitor; MSFI; neutrophil gelatinase-associated lipocalin; NGAL; NGALlipocalin-2; Oncogene 24p3; p25; Siderocalin; Uterocalin

Molecular Weight

Mass (kDA):
22.588 kDA

Genomic Context

Human
Location:	9q34.11
Sequence:	9; NC_000009.12 (128149453..128153453)

Tissue Specificity

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.

Subcellular Localizations

Secreted. Cytoplasmic granule lumen. Cytoplasmic vesicle lumen. 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).

Diseases

• Injury To Kidney
• Acute Kidney Injury
• Kidney Diseases
• Inflammation
• Malignant Neoplasms
• Neoplasms
• Kidney Failure
• Kidney Failure, Chronic
• Carcinoma
• Chronic Kidney Disease
• Obesity
• Cell Invasion
• Insulin Resistance

• Ischemia
• Infective Disorder
• Neoplasm Metastasis
• Heart Failure
• Diabetes Mellitus
• Reperfusion Injury
• Inflammatory Response

Pathways

• Glomerular Filtration
• Excretion
• Secretion
• Pathogenesis
• Inflammatory Response
• Transport
• Immune Response
• Cell Proliferation
• Cell Death
• Localization
• Innate Immune Response
• Neutrophil Activation
• Regeneration

• Cell Differentiation
• Angiogenesis
• Cell Migration
• Cell Cycle
• Reverse Transcription
• Translation
• Endocytosis

PTMs

• Phosphorylation
• Cleavage
• Glycosylation
• Methylation
• Formylation
• Dephosphorylation
• Oxidation

• Demethylation
• Nitrosylation
• Carboxylation
• Bromination
• Biotinylation
• Deacetylation
• Acetylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/LCN2

Boster Bio - Best Uses Of The LCN2 Marker

LCN2 is a growth factor common in astrocytes that are reactive. But what exactly does it mean? Is it a marker of inflammation? What are its best uses and benefits? Read on to find out! Below are some of the best uses for LCN2.

LCN2 is a marker that is found in all to reactive astrocytes

LCN2 causes morphological changes in live and promotes the growth of reactive astrocytes. It regulates iron metabolism and the Bim pathway. These changes could form the basis for self-regulation of reactive Astrocytes. It is interesting to note that LCN2-dependent changes in astrocyte morphology were associated with cell death-sensitive or -prone phenotypes.

Reactive astrocytes secrete inflammatory mediators. Microglia undergoes deramification upon activation and astrocytes expand their processes. These changes are believed to be caused by LCN2 and could be necessary to decrease ON inflammation. In astrocytes, it also increases their susceptibility to the cytotoxic stimuli. This effect was not reproducible in all experiments however, it was minimal.

Reactive astrocytes release LCN2 in response to inflammatory stimuli. LCN2 is also released under conditions of inflammation by astrocytes. The neutralization of LCN2 in cells prevents the induction of changes in morphology. These results suggest that LCN2 has a dual function in controlling cell death as well as the morphology of Astrocytes.

The current study demonstrated that LCN2-immunoreactive cells of astrocytes were significantly larger than C3-immunoreactive cells. LCN2-immunoreactive Astrocells also showed an increase in expression of S100A10, and HuNu. Based on their LCN2 and C3 immunoreactivity the astrocytes with an LCN2-immunoreactive immune response could divided into three groups: medium, low or high.

Overexpression of LCN2 significantly increases the levels of iNOS in the infarcted area of the brain and enhances the expression of GFAP. Furthermore, LCN2 expression was higher in the ischemic part of the brain in mice with LCN2 knockout. In addition, overexpression LCN2 increased the size of the infarct as well as the severity of neural function damage. This suggests that LCN2 may be involved in the process of polarization.

LCN2 has been proven to regulate astrocytes through upregulation of glial fibrosilary acidsic protein (GFAP). In addition, the death caused by LCN2 of astrocytes might affect the activity of Bcl-2 family members. Additionally, LCN2 upregulated Bim expression in C6 glia cells as well as primary astrocytes.

One study demonstrated that LCN2 was expressed when stereotaxically transplanted stereotaxically into naive C57BL/6 mice within 3D LUHMES neurons. MAP2 and HuNu staining demonstrated that LCN2-immunoreactive nerves were present in the striatum on day one of the transplant. On days three, five, and seven, astrocytes that were LCN2-immunoreactive were significantly more responsive than LCN2-/ mice.

LCN2 is linked to iron metabolism, which is intriguing. Two compounds, the iron donor ferric citrate and the chelator feroxamine reduce the death of astrocytes caused by LCN2. A siderophore iron compound also prevented the LCN2-induced cell death sensitization. It is possible that LCN2 could be involved in iron homeostasis.

There is much debate about the exact functions of astrocytes. The study also revealed two distinct astrocyte types one of which is beneficial for neurons that are in anoxic conditions, the other is beneficial to anoxic neuron function. This research has opened up new ways to understand how astrocytes act as mediators of inflammation. It will aid in the development of new therapies for CNS-related diseases.

It could be a sign for inflammation

A new blood test by Boster Bio claims to determine the presence of the protein TNF alpha, a multifunctional proinflammatory cytokine. The protein is part of the tumor necrosis factor superfamily, and its expression is controlled by specific receptors. It is implicated in various diseases such as arthritis, diabetes, as well as insulin resistance. Studies on knockouts in mice suggest that this protein may have a protective function in the brain.

It is a key growth factor

The Anti-Fibroblast Growth Factor 4 FGF4 Antibody from Boster Bio reacts with human FGF4 in ELISA, ICC, and IF assays. This antibody is raised against a synthetic FGF4 peptide and recognizes the final 50 amino acids in the protein. You can also purchase blocking peptides in various lengths for specific immunogens.

FGF-2 is found in a variety of tissues and is involved in a wide spectrum of pathological and physiological processes. Human FGF-2 has 96 percent amino-acid sequence homology rats and mice. It is part of the FGF family. The growth factors have many neurotrophic, mitogenic, and other activities. FGF-1 and FGF-2 are found at high levels in the CNS and exert their cytotrophic effects. FGF-1 and 2 are expressed in all cells, however, they are not found in high levels in other tissues.