NGAL antibody
- Known as:
- NGAL (anti-)
- Catalog number:
- 10-1790
- Product Quantity:
- 200 ul
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- NGAL antibody
Related genes to: NGAL antibody
- Gene:
- LCN2 NIH gene
- Name:
- lipocalin 2
- Previous symbol:
- -
- Synonyms:
- NGAL, 24p3
- Chromosome:
- 9q34.11
- Locus Type:
- gene with protein product
- Date approved:
- 1994-04-29
- Date modifiied:
- 2016-10-05
- Gene:
- SLC22A17 NIH gene
- Name:
- solute carrier family 22 member 17
- Previous symbol:
- -
- Synonyms:
- BOCT, BOIT, NGALR
- Chromosome:
- 14q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-24
- Date modifiied:
- 2015-12-08
Related products to: NGAL antibody
Related articles to: NGAL antibody
- Early apoptosis of grafted islets is one of the critical challenges that significantly impact the efficacy of islet transplantation. We employed Staurosporine to pre-induce apoptosis in bone marrow mesenchymal stem cells (BMSCs). The conditioned medium from apoptotic BMSCs was then used to pretreat β cells, which notably enhanced the suppression of β cell apoptosis. For in vivo experiments, co-transplantation of islets and apoptotic BMSCs under the renal capsule of diabetic rats inhibited islets apoptosis and resulted in better transplantation outcomes. Subsequently proteomic analysis revealed that the iron-loaded form of Lcn2 protein (holo-Lcn2) secreted by apoptotic BMSCs played a crucial role in exerting anti-apoptotic effects. Holo-Lcn2 binds to the Slc22a17 transporter on cell membrane, facilitating the transport of Fe into cells. Inhibition of Fe transport suppressed the anti-apoptotic effect of holo-Lcn2. Thus, we hypothesize that apoptotic BMSCs reduce grafted islets apoptosis through the holo-Lcn2/Slc22a17/Fe axis. This study provides insights into the application of BMSCs-based acellular therapies in islet transplantation. - Source: PubMed
Publication date: 2026/04/10
Lu CuinanWang JialeWang YingWang JingwenBi HuanjingYu XiaoyangChen ZuhanDong BoqingMa RuiyangDing Xiaoming - - Source: PubMed
Publication date: 2026/04/10
Jiang LiHou Yun-FanMao Yan-TingHuang Si-MinWang YuNi KunYao YueYu Jia-ChengHuang Yu-LinXu RuiZhang WeiGu Xiao-PingMa Zheng-Liang - Viral mimicry, i.e., the ability of uninfected cancer cells to emit molecular signals normally associated with infection, is paramount for anticancer immunity. Recent findings from Bossowski et al. indicate that the integrated stress response (a crucial component of cellular responses against infection) can unexpectedly promote immune evasion via an LCN2-driven, macrophage-dependent mechanism. - Source: PubMed
Publication date: 2026/04/01
Borriello LuciaGalluzzi Lorenzo - Osteocytes, the most abundant bone cells, are central regulators of bone remodeling that also exert endocrine control over systemic metabolism. Among the factors they produce, Lipocalin-2 (LCN2) has emerged as a cytokine linking bone and energy homeostasis, yet its local role within the skeleton remains elusive. Here, we identify that LCN2 promotes intracellular iron accumulation, mitochondrial dysfunction, and lipid peroxidation through its receptor SLC22A17, and drives ferroptotic cell death. Dmp1-Cre-mediated deletion of Lcn2 preserves mitochondrial integrity, reduces intracellular iron and lipid peroxidation, and enhances osteocyte dendricity and lacunocanalicular connectivity. Mechanistically, loss of Lcn2 suppresses Wnt antagonists DKK1 and SOST, thereby promoting Wnt/β-catenin signaling and stimulating osteoblast-mediated bone formation. Notably, Dmp1-Cre-mediated deletion of Lcn2 does not alter systemic energy balance, underscoring LCN2's local skeletal function. These findings define the LCN2-SLC22A17 axis as a local regulator of osteocyte ferroptosis, Wnt/β-catenin signaling, and skeletal fragility. - Source: PubMed
Publication date: 2026/02/25
Khanal VivekCarroll MadelineMoradi FatemehCarter JaydenZhong YingShashank Chikkamagaluru GSato Amy YAllen Ryan MWankhade Umesh DDole Neha S - Brain metastasis is a major contributor to mortality in patients with lung cancer. The unique microenvironment of the brain plays a critical role in the initiation and progression of brain metastases (BM), yet the molecular mechanisms underlying tumor-microenvironment interactions remain poorly understood. Here, we demonstrate that upregulation of lipocalin-2 (LCN2) in tumor cells promotes brain metastatic progression by orchestrating crosstalk among metastatic tumor cells, astrocytes, and macrophages. Brain metastatic tumor cells secrete LCN2, which binds to SLC22A17 on astrocytes, activating JAK2/STAT3 signaling and inducing astrocyte activation and chemokine secretion, thereby facilitating macrophage recruitment. In turn, macrophages secrete IL-1β, which further upregulates LCN2 expression in tumor cells. Prophylactic administration of the IL-1 receptor antagonist anakinra inhibits BM formation, whereas therapeutic administration alone is ineffective. However, treatment with the STAT3 inhibitor SH4-54, either alone or in combination with anakinra, significantly suppressed tumor growth in the BM. Furthermore, tumor-secreted LCN2 can bind to SLC22A17 on tumor cells, activating JAK2/STAT3 signaling and promoting VEGF-A expression and release, which enhances tumor neovascularization. Inhibition of this axis with SH4-54, bevacizumab, or their combination effectively reduces the tumor burden in BM-bearing mice. These findings underscore the central role of LCN2 in driving brain metastasis and highlight a potential therapeutic strategy for targeting brain metastatic lung cancer. - Source: PubMed
Publication date: 2025/12/24
Zhu YixiangZhang JianHe DanmingCai HongqingHe YanYuan LiLi SiniDong YuchengZhuang WeiWang ZhijieDuan JianchunZhang XueMa ZixiaoBai HuaWang Jie