NGAL antibody
- Known as:
- NGAL (anti-)
- Catalog number:
- 10-1798
- 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
- Prostate cancer (PCa) is a hormone-dependent tumor and one of the most prevalent cancers in men worldwide. PCa progression is influenced by its interaction with the surrounding tumor microenvironment, highlighting the role of periprostatic adipose tissue (PPAT), which modulates PCa behavior through the secretion of bioactive molecules (e.g., adipokines). However, the influence of this complex cell communication, particularly under altered metabolic conditions, remains to be fully elucidated. - Source: PubMed
Publication date: 2026/05/14
Pérez-Gómez Jesús MPrats-Escribano AntonioGil-Duque IgnacioArroyo-Millán LauraHuertas-Cabrera HugoNúñez-Santos Miguel ALópez-Ruiz Daniel JMata-Ordoñez FernandoGonzález-Serrano TeresaOrtea IgnacioPorcel-Pastrana FranciscoÁlvarez-Benito MarinaPlanque MélanieCarrasco-Valiente JuliaGómez-Gómez EnriqueGuzmán-Ruiz RocíoFuentes-Fayos Antonio CFendt Sarah-MariaGahete Manuel DSarmento-Cabral AndréMalagón María Del MarLuque Raúl M - 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 - Cancer-related pain and anxiety significantly negate the quality of life in patients. Oligodendrocyte precursor cells (OPCs) were reported to involve in engulf synapses and remodel neural circuits. This study aimed to elucidate the role of OPCs-mediated phagocytosis of GABAergic synapses in a mouse model of bone cancer pain. Male C3H mice were utilized to establish a model of bone cancer pain. In vivo fiber photometry was used to monitor the activity of GABAergic neurons, and chemogenetic techniques were applied to modulate neuronal excitation. The phagocytosis of GABAergic synapses by OPCs was visualized via immunofluorescence-based 3D reconstruction and immunoelectron microscopy. Interventions targeting lipocalin-2 (LCN2) and its receptor SLC22A17 were carried out with adeno-associated virus (AAV), siRNA, and pharmacological tools. On the 21st postoperative day, mice with bone cancer displayed significant pain and anxiety-like behaviors. Tumor-bearing mice exhibited a compensatory increase in calcium activity among GABAergic neurons within the anterior cingulate cortex (ACC). Compared with sham-operated mice, OPC phagocytosis of GABAergic synapses was higher in the tumor-bearing mice than controls. Concurrently, a pronounced upregulation of LCN2 expression was observed in the tumor group. Administration of LCN2-neutralizing antibodies or AAV-mediated intervention markedly alleviated pain and anxiety-related behaviors in mice with bone cancer. Moreover, the LCN2 receptor SLC22A17 expression was significantly increased. Targeted inhibition of SLC22A17 induced cytoskeletal remodeling and decreased their phagocytic capacity of OPCs. Collectively, LCN2/SLC22A17 signal was involved in OPCs-mediated phagocytosis of GABAergic synapses and contributed to cancer pain and anxiety development. - 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